Tick Management Handbook A integrated guide for homeowners, pest control operators, and public health officials for the prevention of tick-associated disease Prepared by: Kirby C. Stafford III Chief Scientist The Connecticut Agricultural Experiment Station, New Haven

Produced as part of the Connecticut community-based Lyme disease prevention projects in cooperation with the following Connecticut health agencies: The Connecticut Department of Public Health The Westport Weston Health District The Torrington Area Health District The Ledge Light Health District Funding provided by

The Centers for Disease Control and Prevention The Connecticut Agricultural Experiment Station

This handbook was developed as part of a community-based program for the prevention of tickborne illness supported through a cooperative agreement with the Centers for Disease Control and Prevention (CDC). The CDC funded publication of this tick handbook. A series of tick and tickassociated disease information sheets first developed by Dr. Kirby Stafford at the Connecticut Agricultural Experiment Station in 1992 and updated and expanded periodically was the original basis for this handbook.

Acknowledgements Thanks are given to Dr. Joseph Piesman (CDC, Fort Collins, Colorado), Dr. Peter J. Krause (University of Connecticut Health Center, Farmington, Connecticut), Carol Lemmon (CAES, retired), Bradford Robinson (Connecticut Department of Environmental Protection, Pesticide Management Division), Judith Nelson, Director, and the staff of the Westport Weston Health District (CT), Dr. Terry Schulze (NJ), Dr. Gary Maupin (CDC, retired), and Drs. Louis A. Magnarelli and John F. Anderson (CAES) for reviewing parts or all of this handbook. Their comments and suggestions were sincerely appreciated. Thanks are also extended to Vickie Bomba-Lewandoski (CAES) for publication and printing assistance.

Photo Credits Many of the pictures and illustrations are those of the author or staff at the Connecticut Agricultural Experiment Station (CAES). Sources other than the author are numbered or otherwise noted in captions. Sincere thanks are given to the following for permission to use their photographs or illustrations and federal government sources are also gratefully acknowledged. Pfizer Central Research (Groton Point Road, Groton, CT): 1, 6, 7, 8, 9, 11, 12, 20, 21, 23, 24, 25, 26, 32, 33, 34, 37, 47, 48. Centers for Disease Control and Prevention: 13, 14, 16, 17, 19, 27, 28, 29, 30, 36, risk map. United States Department of Agriculture: Cover (tick), tick morphology figure (adapted from Strickland et al. 1976), 39. American Lyme Disease Foundation (Somers, NY): 3, 4, 10, 43. Barnstable County Cooperative Extension (Massachusetts): 40. Vector-borne Disease Laboratory, Maine Medical Center Research Institute (Portland, ME): 15. Bayer Environmental Science (Montvale, NJ): 46. United Industries (Spectrum Brands): 38. Ric Felton (Goshen, CT; www.semguy.com): 35. Jim Occi (Cranford, NJ): 5, 18, 45. Lynne Rhodes (Old Saybrook, CT): 22, 23. Steven A. Levy, DMV (Durham, CT): 31. CAES: Jeffrey S. Ward, 2; Uma Ramakrishnan, 41, 42; and Jeffrey Fengler, 44.

Disclaimer Mention of a product or company is for informational purposes only and does not constitute an endorsement by the Connecticut Agricultural Experiment Station. Published Summer 2004  2004 The Connecticut Agricultural Experiment Station

Table of Contents Introduction ..........................................................................................................................................................1 Ticks of the Northeastern United States.............................................................................................................3 Tick biology and behavior...............................................................................................................................4 Tick morphology .............................................................................................................................................6 Blacklegged tick, Ixodes scapularis ................................................................................................................7 American dog tick, Dermacentor variabilis..................................................................................................10 Lone star tick, Amblyomma americanum ......................................................................................................12 Other ticks .....................................................................................................................................................13 Tick-Associated Diseases....................................................................................................................................15 Lyme disease .................................................................................................................................................15 Southern Tick-Associated Rash Illness .........................................................................................................21 Human Babesiosis .........................................................................................................................................21 Human Ehrlichiosis .......................................................................................................................................23 Rocky Mountain Spotted Fever.....................................................................................................................24 Tick Paralysis ................................................................................................................................................25 Tularemia ......................................................................................................................................................26 Powassan Encephalitis ..................................................................................................................................26 Tick-borne Relapsing Fever ..........................................................................................................................27 Colorado Tick Fever......................................................................................................................................27 Bartonella Infections .....................................................................................................................................27 Lyme Disease in Companion Animals ..............................................................................................................28 Personal Protection ............................................................................................................................................29 Tick bite prevention ......................................................................................................................................29 How a tick bites & feeds ...............................................................................................................................31 Tick removal .................................................................................................................................................32 Repellents......................................................................................................................................................34 Integrated Tick Management ............................................................................................................................37 Landscape management ................................................................................................................................39 Management of host animals.........................................................................................................................43 Prevention of tick-associated disease in companion animals ........................................................................51 Backyard Wildlife programs and environmentally friendly lawns................................................................52 Area-wide Chemical Control of Ticks ..............................................................................................................53 Acaricides used for tick control.....................................................................................................................54 Homeowner application of acaricides ...........................................................................................................55 Commercial application of acaricides ...........................................................................................................56 An acaricide primer .......................................................................................................................................58 Organic Landcare Practices ..............................................................................................................................60 Biological Control...............................................................................................................................................60 Selected Bibliography.........................................................................................................................................61

To these I must add the wood lice [ticks] with which the forests are so pestered that it is impossible to pass through a bush or to sit down, though the place be ever so pleasant, without having a whole swarm of them on your clothes. Pehr Kalm, 18 May 1749 Raccoon [Swedesboro], New Jersey

Introduction Ticks have become an increasing problem to people and animals in the United States. Ticks are obligate blood-feeders that require an animal host to survive and reproduce. They feed on a wide variety of mammals, birds, reptiles, and even amphibians. While most ticks feed on specific host animals and are not considered to be of medical or veterinary importance, several ticks have a wide host range and attack people, pets, or livestock. Ticks can be a nuisance; their bites can cause irritation and, in the case of some ticks, paralysis. Severe infestations on animals can cause anemia, weight loss, and even death from the consumption of large quantities of blood. Ticks can also transmit many human and animal disease pathogens, which include viruses, bacteria, rickettsiae, and protozoa. The association between ticks and disease was first demonstrated when Theobald Smith and Fred Kilbourne proved in 1893 that Texas cattle fever (cattle babesiosis) was caused by a protozoan transmitted by an infected tick. In the late 1800s, Rocky Mountain spotted fever was the first human tick-borne disease identified in the United States and for many years was the major tick-associated disease in this country. Although first recognized from the virulent cases in the Bitterroot Valley of Montana, it eventually became evident that most cases were distributed through the eastern United States. Lyme disease was first recognized as a distinct clinical entity from a group of arthritis patients in the area of Lyme, Connecticut, in 1975, although it became evident that this disease had an extensive history in Europe throughout the twentieth century. Today, Lyme disease is the leading arthropod-associated disease in the United States with over 23,000 human cases reported to the Centers for Disease Control and Prevention (CDC) in 2002. This may represent only about 10% of physician-diagnosed cases. Surveys have found that up to a quarter of residents in Lyme disease endemic areas have been diagnosed with the disease and that many residents perceive the disease as a serious or very serious problem. Without an effective intervention strategy, the steadily increasing trend in Lyme disease case reports is likely to continue. In the northeastern United States, the emergence of Lyme disease can be linked to changing landscape patterns. A Swedish naturalist named Pehr Kalm recorded in his journal of his travels in the United States in 1748-1750 that ticks were abundant and 1

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In Thousands

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Estimated Deer Numbers in Connecticut

60 40 20 0 1880 1900 1920 1940 1960 1980 2000

annoying. Over a century later in 1872, entomologist Asa Fitch noted that ticks were nearly or quite extinct along the route that Pehr Kalm had traveled. During this time, the land had been cleared for agriculture and white-tailed deer in many areas were drastically reduced or virtually eliminated due to habitat loss and unregulated hunting. With the reestablishment of forested habitat and animal hosts through the latter half of the twentieth century, ticks that may have survived on islands off the southern New England coast were able to increase and spread. The blacklegged tick, Ixodes scapularis, which is commonly known as the “deer” tick, and the principal vector for Lyme disease spirochetes, was present on Naushon Island, Massachusetts, in the 1920s and 1930s. Some I. scapularis from Montauk Point, Long Island, New York, that were collected in the late 1940s and early 1950s were found infected with Lyme disease bacteria. The risk of human infection increased through the 1960s and 1970s until the recognition of the disease from the cluster of cases in Lyme, Connecticut, in 1975. The rising incidence of Lyme disease is due to a number of factors including: • Increased tick abundance • Overabundant deer population • Increased recognition of the disease • Establishment of more residences in wooded areas • Increased the potential for contact with ticks. An estimated three quarters of all Lyme disease cases are acquired from ticks picked up during activities around the home. With the steady increase in the incidence and geographic spread of Lyme disease, there is a need for homeowners, public health officials, and the pest control industry to learn how to manage or control the tick problem. The withdrawal of the human Lyme disease vaccine (LYMErix) has essentially brought the control of the disease back to managing tick bites and methods to suppress the local tick population or prevalence of pathogen infection in the ticks. The purpose of this handbook is to provide basic information on ticks and their biology, basic information on the diseases they carry, methods to reduce the risk of exposure to these parasites, and most importantly, information on how to reduce or manage tick populations, and therefore risk of disease, in the residential landscape.

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Ticks: the foulest and nastiest creatures that be. Pliny the Elder, 23-79 A.D.

Ticks of the Northeastern United States Ticks are not insects, but are arthropods more closely related to mites, spiders, scorpions, and daddy-long-legs. There are about 80 species of ticks in the United States (850 species worldwide). However, only about 12 or so in the U.S. are of major public health or veterinary concerns with a few others that occasionally attack humans. The ticks discussed in this handbook belong to the family Ixodidae or hard ticks. The principal hard ticks recovered from humans in the mid-Atlantic and northeastern United States are the blacklegged (i.e., deer) tick, Ixodes scapularis, the American dog tick, Dermacentor variabilis, and the lone star tick, Amblyomma americanum. Other tick species recorded as feeding on humans in the eastern U.S. include Ixodes cookei, Ixodes dentatus, and the brown dog tick, Rhipicephalus sanguineus. The Argasidae or soft ticks form the other major group of ticks. Soft ticks are generally nest inhabitants that are associated with rodents, birds, or bats. Several species of soft ticks attack humans and can transmit disease, mainly in western states, but are not the focus of this handbook. One species, Carios (Ornithodoros) kelleyi, a bat tick, has been recovered from states in the northeast to at least Connecticut.

Table 1. Important ticks of the northeastern states and some other major ticks of medical importance in the United States. Tick Hard Ticks Ixodes scapularis Ixodes pacificus Ixodes cookei Ixodes dentatus Amblyomma americanum Dermacentor variabilis Dermacentor andersoni Dermacentor albipictus Rhipicephalus sanguineus Soft Ticks Ornithodoros species ticks Carios kelleyi

Common name

General distribution

Blacklegged tick Western blacklegged tick A woodchuck tick A rabbit tick Lone star tick American dog tick Rocky Mountain wood tick Winter tick Brown dog tick

Northeastern & mid-western United States Pacific coast & parts Nevada, Arizona, Utah Eastern United States & northeast Canada Eastern United States Southeastern U.S., Texas to New York Eastern U.S. & west coast Rocky Mountain states south to NM & AZ Canada, United States south to Central America All U.S. and worldwide

Relapsing fever ticks A bat tick

Western United States Widespread in U.S., north to New York and Connecticut

Scientific Names and a Few Terms The scientific name of ticks, like other organisms, is given in two parts: genus (capitalized, often abbreviated by the first letter, e.g. I. scapularis) and species (not capitalized) sometimes followed by the name of the person who described the organism (given in parenthesis if the genus name is later changed). The name Linneaus is abbreviated L. Common names like deer tick can vary regionally and some organisms may have no common name. The common names used in this guide follow those officially recognized by scientific societies. Several terms are used to define the cycles of animal, tick and pathogen. •

Pathogen: the microorganism (i.e., virus, bacteria, rickettsia, protozoa, fungus) that may cause disease.

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Parasite: An animal that lives in or on a host for at least part of their life and benefits from the association at the expense of the host (from the Greek, literally para - beside and sitos - food).

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Vector: An insect or other arthropod, like a tick, that carries and transmits a disease pathogen. Diseases associated with pathogens transmitted by a vector are called vectorborne diseases.

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Host: An animal infected by a pathogen or infested with a parasite.

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Reservoir: An animal host that is capable of maintaining a pathogen and serving as a source of infection.

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Zoonoses: A disease caused by a pathogen that is maintained in vertebrate animals that can be transmitted naturally to humans or domestic animals by a vector or through other means (e.g. saliva, feces).

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Endemic disease: A disease that is established and present more or less continuously in a community.

Tick Biology and Behavior Ticks are essentially mites that have become obligate blood-feeders, requiring a host animal for food and development. Ticks have four stages in their life cycle: egg, the 6-legged larva (seed ticks), and 8-legged nymph and adult (male or female). Larvae and nymphs change to the next stage after digesting a blood meal by molting or shedding the cuticle. Most of the ticks mentioned in this handbook have a 3-host life cycle, whereas each of the three active stages feed on a different individual host animal, taking a single blood meal. Larvae feed to repletion on one animal, drop to the ground and molt to a nymph. The nymphs must find and attach to another animal, engorge, drop to ground and molt to an adult. The adult tick feeds on a third animal. A replete or engorged (blood filled) female tick produces a single large batch of eggs and dies. Depending upon the species of tick, egg mass deposited can range roughly from 1,000 to 18,000 eggs.

3-host tick life cycle

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Larvae

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Nymphs

Adults

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Engorged female laying eggs

The larvae and nymphs generally feed on small to medium-sized hosts, while adult ticks feed on larger animals. Some ticks may have a one-host (all stages staying and feeding on only one animal host before the female drops off) or other multi-host lifecycles. Depending upon the tick, the life cycle may be completed in 1, 2 or even 3 years, while a one-host tick may have more than one generation per year. Feeding for only a few days, the majority of the life of a tick is spent off the host in the environment either seeking a host, molting or simply passing through an inhospitable season (e.g., hot summers or cold winters). Soft ticks have a multi-host life cycle with multiple nymphal stages; each stage feeds briefly, and adults take multiple small blood meals, laying small egg batches after each feeding. As nest and cave dwellers, often with transient hosts, some argasid ticks may survive many years without a host. However, most hard ticks do not successfully find a host and perish within months or a year or two at best.

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Larval ticks will be clustered on the egg mass after hatching and when ready to feed, ascend blades of grass or similar vegetation to await a host. Ticks assume a questing position by clinging to the leaf litter or vegetation with the back legs, and hold the first pair outstretched. Due to differences in susceptibility to desiccation and host preference, immature ticks generally remain in the low vegetation, while adult ticks may seek a host at a higher level in the vegetation. Ticks detect their hosts through several host odors (including carbon dioxide, ammonia, lactic acid, and other specific body odors), body heat, moisture, vibrations, and for some, visual cues like a shadow. When approached by a potential host, a tick becomes excited - waving the front legs in order to grab the passing host. Ticks cannot fly or jump; they must make direct contact with a host. Once on a host a tick may attach quickly or wander over the host for some time. Some ticks attach only or principally on certain areas like the ear or thin-skinned areas, while other species may attach almost anywhere on the host. Ticks feed slowly, remaining on the host for several to many days, until engorged with blood (see section on feeding in tick bite prevention). Male ticks feed intermittently, take small blood meals, and may remain on a host for weeks. For most ticks mating occurs on the host, as the male tick also requires a blood meal. However, male Ixodes ticks do not need to feed prior to mating and mating may occur on or off the host.

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Tick Morphology The body of a tick consists of a “false head” (the capitulum) and a thorax and abdomen fused into a single oval, flattened body. A larval tick has six legs, while nymphs and adults have eight legs present. The basal segment of the leg, the coxa, may have spurs that help in identification. An adult tick will have a genital aperture on the ventral surface, located roughly between the second pair of legs. The respiratory system is evident by spiracular plates located ventrolaterally behind the fourth pair of legs in the nymphs and adults. These plates may be oval, rounded, or comma-shaped. Hard ticks get their name from a tough dorsal shield or plate called the scutum present on all mobile stages of the tick. The scutum on the larva, nymph, and female tick covers the dorsal anterior third to half of the body. By contrast, the scutum on a male tick covers almost the entire dorsal surface and expansion during feeding is very limited. The scutum differs in shape and others characteristics (i.e., presence or absence of simple eyes) between tick genera. In some ticks, ornate or patterned markings may be present that can aid in identification. A distinct semicircular anal groove curves around the front of the anal opening in Ixodes ticks. In all other ticks, the anal groove is behind the anus or absent. Many ticks, but not Ixodes, have rectangular areas separated by grooves on the posterior margin of the tick body called festoons. Festoons, if present, may not be visible on fully engorged females. Argasid ticks are leathery, wrinkled and grayish in appearance. The capitulum of soft ticks is located on the underside of the body and cannot be seen from above.

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The capitulum in hard ticks is visible dorsally in all stages. The capitulum holds the mouthparts consisting of a base (basis capituli), two palps, paired chelicerae, and the median ventral hypostome, which is covered with denticles or recurved teeth. The shape of the basis capituli, length of the palps, number of denticles, and other characteristics of the mouthparts are used to help identify tick genera and species. While the adults of some common ticks can be easily identified with a little training because of distinctive markings or color, the identification of most ticks and the immature stages requires the services of a trained entomologist and the use of keys developed by tick taxonomists. These keys are designed to specifically identify adults, nymphs or larvae.

The Blacklegged Tick or “Deer” Tick, Ixodes scapularis Say Blacklegged tick is the correct common name for the tick popularly known as the “deer” tick (the terms are not used together, it is not called the blacklegged deer tick). Ixodes (pronounced ix-zod-ease) scapularis transmits the causal agents of three diseases; Lyme disease, human babesiosis, and human anaplasmosis. The blacklegged tick is found from some southern portions of Canada and coastal Maine through the midAtlantic states into Maryland, Delaware and northern parts of Virginia and in several Above: left to right: larva, nymph, male and female I. north central states, particularly Wisconsin scapularis. Below top: unfed and engorged female. Below bottom: male, female and engorged female with straight pin. and Minnesota, extending down through Illinois and into Indiana. This tick is also found throughout the southeastern United States west to southcentral Texas, Oklahoma, southern Missouri, and eastern Kansas. However, few I. scapularis in the southeast have been found infected with the bacterium that causes Lyme disease, the spirochete Borrelia burgdorferi. Therefore, the risk for Lyme disease from this tick in the southeastern United States is considered relatively low. Unfed female I. scapularis have a reddish body and a dark brown dorsal scutum (plate) located behind the mouthparts. Length of the female tick from the tip of the palpi to the end of the body is about 3 to 3.7 mm (about 1/10 of an inch). Male I. scapularis are smaller (2 – 2.7 mm) than the female and are completely dark brown. Nymphs are 1.3 to 1.7 mm in length, while larvae are only 0.7 to 0.8 mm. Female blacklegged ticks become fairly large when engorged with blood and, consequently, are sometimes confused with engorged female American dog ticks.

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Blacklegged ticks feed on a wide variety of mammals and birds, requiring 3-7 days to ingest the blood, depending on the stage of the tick. Larvae and nymphs of I. scapularis typically become infected with B. burgdorferi when they feed on a reservoir competent host. The white-footed mouse is the principal reservoir (source of infection) for B. burgdorferi, the protozoan agent of human babesisois, Babesia microti, and can serve as a reservoir for the agent of human granulocytic ehrlichiosis. Birds are also a major host for immature I. scapularis and have been implicated in the longdistance dispersal of ticks and B. burgdorferi. Whitetailed deer, Odocoileus virginianus (Zimmerman), are the principal host for the adult stage of the tick, which feeds on a variety of medium- to large-sized mammalian hosts. An engorged female tick may typically lay around 2,000 eggs or more. Below clockwise from top left: Nymphal I. scapularis in the hand, close-up of an I. scapularis nymph (fingerlike projections of the tick mid-gut where the Lyme spirochetes are found are visible through the tick cuticle), female and nymph I. scapularis on finger, and nymphal I. scapularis on finger.

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The Lyme disease spirochete in northern states is maintained, in part, by the two-year life cycle of the tick. Seasonally, the nymphs precede larvae and infect a new generation of animal hosts. Larvae 8

active later in the summer then become infected when feeding on reservoir host animals. Adults of I. scapularis are more commonly infected with B. burgdorferi than the nymphs because the tick has had two opportunities to become infected, once as a larva and once as a nymph.

Two-year Life Cycle for Ixodes scapularis. 3. Nymphs attach & feed on small mammals and birds bird

2. Larvae hatch and feed

1. Engorged females lay eggs

June

July

August September

May ay

October April November March February December January

5. Adult ticks active warm days winter with second peak of activity in spring

Nymphs Overwinter

4. Adults seek medium to large mammalian hosts, primarily deer

Seasonal activity of I. scapularis adults, nymphs, and larvae. A d u lt

N ym ph

L a rv a

Jan

Feb

M ar

Apr

M ay

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O ct

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D ec

The American Dog Tick, Dermacentor variabilis (Say) The American dog tick, Dermacentor variabilis, is the primary vector of the causal agent of Rocky Mountain spotted fever in the eastern United States and is also a vector for the agent of tularemia. This tick does not transmit Lyme disease spirochetes and recent studies have indicated that it is not a vector for the agent of human granulocytic ehrlichiosis. The American dog tick, known by some people as the wood tick, is one of the most widely distributed and common ticks in the eastern and central United States, found from Nova Scotia to the Gulf Coast as far west as Texas, Kansas and the Dakotas. It is also found in parts of California, Oregon, eastern Washington, and northern Idaho. Only adults of the American dog tick feed on people and their pets – records of nymphs from humans are rare. The Rocky Mountain Wood tick, Dermacentor andersoni, is found in western North America from British Columbia and Saskatchewan south through North Dakota to northern New Mexico and Arizona and California. This tick is the vector for Rocky Mountain spotted fever and Colorado tick fever in western Canada and the northwestern United States. Adult American dog ticks are reddish brown in color with silvery-gray or whitish markings on the back or upper body. They are almost 6.4 mm (¼ inch) in length. The palps are short. The ornate marking are on the scutum of the female and on the male extend over the entire back. Female ticks increase dramatically in size as they obtain their blood meal from a host animal. Fully engorged females may reach ½ inch in length (13 mm long by 10 mm wide) and resemble a dark pinto bean. Male ticks do not change notably in size as they feed. The scutum or plate does not change in size and the white markings are readily visible on a blood-fed tick. Adult dog ticks can be distinguished from adult I. scapularis by their larger size and the white markings on the dorsal scutum. In the northeast, adults of both tick species are active during the spring. Dogs are the preferred hosts of adult ticks, but they also feed readily on other medium to large mammals. These include opossums, raccoons, skunks, fox, coyote, bobcat, squirrel, cattle, sheep, horses and people. Larvae and nymphs of the American dog tick feed on meadow voles (Microtus pennsylvanicus), whitefooted mice (Peromyscus leucopus), and other rodents. In New Jersey, adult ticks are active from mid-March to mid-August. In Connecticut and Massachusetts, adults become active about midApril to early May, peak in June, and may remain a nuisance until mid-August. Mating occurs on the host. A female tick will feed for 10-12 days. Once she is engorged with blood, she drops off the host, and may deposit about 3,000 to 7,000 eggs (average around 5,000). Males continue to ingest small amounts of blood from the host. In the northeast, the American dog tick probably requires 2 years to complete its life cycle as opposed to one year in the southern parts of its range. American dog ticks can live for extended periods without feeding, more than two years to almost three years, if suitable hosts are not available. Larvae, nymphs, and adults may live up to 540, 584, and 1,053 days, respectively, although typically survival will be much less.

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American dog ticks are most numerous along roadsides, paths, old fields, marshy areas and trails in brushy woodlands or meadows with tall grass or weeds. Meadow voles are found in fields, pastures, fresh and saltwater marshes and meadows, borders of streams and lakes, and open and wooded swamps. Consequently, large numbers of American dog ticks may be encountered in these areas. People or their pets may bring these ticks from outdoors into the home, where they can survive for many days. However, the tick will not become established indoors. The Brown dog tick (page 13) is the species that may cause household infestations.

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Comparison between the blacklegged tick and American dog tick (above). Top row left to right: nymph, male, female, and engorged female I. scapularis. Note engorged female is nearly as large as the engorged female American dog tick. Bottom row left to right: male, female, and engorged female D. variabilis. Note the white markings on the scutum of D. variabilis can help distinguish between the two engorged ticks (ruler is marked in 1/16 inch intervals between the 1 and 2 inch mark).

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The Lone Star Tick, Amblyomma americanum (L.) The lone star tick, Amblyomma americanum, is named from the conspicuous spot on the end of the scutum of the female tick. This tick is the vector for Ehrlichia chaffeensis, the agent of human monocyctic ehrlichiosis (HME). The tick does not transmit the Lyme disease bacterium, B. burgdorferi, but has been linked with a Lyme-like illness with a rash and other symptoms resembling Lyme disease called southern tick-associated rash illness or STARI. Possibly caused by another species of spirochete, attempts to culture 16 the organism from skin biopsies at the rash or obtain serological evidence of Lyme disease from affected patients have not been successful thus far. A new spirochete, B. lonestari, has been described from lone star ticks based on a DNA analysis and has recently been cultured from ticks. It has been detected in both a tick and associated rash, but it is yet not clear if it is the agent of the Lyme-like illness. The lone star tick is widely distributed through the southeastern United States as far west as Texas and north to southern parts of Iowa, Illinois, Indiana, Ohio, and Pennsylvania. Along the Atlantic coast, its northern range extends to New Jersey and Long Island, New York, and it is also abundant on Prudence Island, Rhode Island. Lone star tick populations in Connecticut are sparse, but these ticks are occasionally recovered from residents, mainly in coastal communities in Fairfield and New Haven Counties.

Approximate distribution of A. americanum shown in green shaded area.

Lone star ticks are reddish brown in color and about 3 to 4 mm long. The palps of Amblyomma ticks are long. Female ticks have a conspicuous spot on the end of the scutum. Male ticks have faint white markings at the edge of the body. Nymphs are more circular in shape than I. scapularis nymphs and reddish in tint. Adults are active in the spring, while nymphs are active from April through the mid-summer. Larvae are active in the late summer and early fall. The lone star tick has a wide host range, feeding on virtually any mammal. All stages will feed on people. On wild hosts, feeding occurs principally in and on the ears and the head. The bite of this tick can be painful because of the long mouthparts and attached ticks can cause great irritation. All stages are active during the summer months. Female ticks can deposit 1,000 to 8,000 eggs with an average of around 3,000 eggs. Deer and other large to medium sized animals are hosts for the adults and nymphs. Heavy infestations of this tick have been known to result in blindness and death of fawns of white-tailed deer. In some localities, this tick may also be known as the “deer” tick. Larvae and nymphs commonly feed on large and medium-sized mammalian hosts. Larval ticks also feed on many species of birds. Rodents do not appear to be important hosts for immature A. americanum.

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Other Ticks Ixodes cookei Packard Ixodes cookei, sometimes referred to as the “woodchuck tick”, is found throughout the eastern half of the United States and Canada. It is a primarily a parasite of medium-sized mammals such as woodchucks, opossums, raccoons, skunks, and foxes. In a New York study, it was the second most abundant tick on medium-sized mammals behind I. scapularis. All stages of I. cookei will feed on humans, though reports in southern New England and New York are uncommon. It appears to be a more frequent human parasite in northern New England and Ontario, Canada. After the American dog tick, I. cookei was the second most common tick removed from humans in Maine from 19891990 (I. scapularis was third). Lyme disease spirochetes have been detected in this tick, but laboratory studies suggest it is not a good vector for B. burgdorferi. However, I. cookei is the principal vector for Powassan virus, which can cause severe or fatal human encephalitis.

Brown Dog Tick, Rhipicephalus sanguineus (Latreille) The brown dog tick or kennel tick, Rhipicephalus sanguineus, is a three-host tick found almost worldwide and throughout the United States. The tick is more abundant in the southern states. This is the only species of this genus in the U.S. Domestic dogs are the principal host for all three stages of the tick, especially in the United States, although the tick feeds on other hosts in other parts of the world. Adult ticks feed mainly inside the ears, head and neck, and between the toes, while the immature stages feed almost anywhere, including the neck, legs, chest, and belly. People may occasionally be attacked. This tick is closely associated with yards, homes, kennels and small animal hospitals where dogs are present, particularly in pet bedding areas. In the North, this tick is found almost exclusively indoors. Brown dog ticks may be observed crawling around baseboards, up the walls or other vertical surfaces of infested homes seeking protected areas, such as cracks, crevices, spaces between walls or wallpaper, to molt or lay eggs. A female tick can deposit between 360 to 3,000 eggs. Under favorable conditions, the life cycle can be completed in about two months. This tick is the vector for canine ehrlichiosis (Ehrlichia canis) and canine babesiosis (Babesia canis or Babesia gibsoni). The brown dog tick is a vector for Boutonneuse fever in Europe and Africa.

Winter Tick, Dermacentor albipictus (Packard) The winter tick, Dermacentor albipictus, is a one-host tick found commonly on moose (Alces alces), elk (Cervus elaphus), and deer. Hunters will encounter this tick (as well as I. scapularis) on harvested deer, moose, and elk during the hunting season. Heavy tick infestations can cause anemia and other problems and death of the animal. Larval ticks infest animals in the fall and then develop into nymphs and adults without leaving the host. Engorged females will drop off the host animal in the spring. This tick is broadly distributed from Canada to Central America. This tick will occasionally feed on humans.

Western Blacklegged Tick, Ixodes pacificus Cooley and Kohls Although outside the scope of this handbook, readers should note that the western blacklegged tick, Ixodes pacificus, is the principal vector for Lyme disease to humans in the western United States. It looks just like the blacklegged tick in the east and only a specialist could tell them apart. It is found along the Pacific Coast in the western half of Washington and Oregon, almost all of California, and in parts of Utah, Arizona, and New Mexico. Infection rates with B. burgdorferi are generally low, 5-6% or less, because many of the immature I. pacificus ticks feed on the western fence lizard (Sceloporus occidentalis), a reservoir incompetent host for B. burgdorferi whose blood also contains a borreliacidal factor that destroys spirochetes in I. pacificus nymphs. Several rodents

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(mainly woodrats) and a nest dwelling tick, I. spinipalpis, maintain the enzootic cycle of Lyme disease in California and other western states.

Carios (Ornithodoros) kelleyi Cooley and Kohls This tick feeds on bats and is found in homes, bat colonies, and other areas where bats may be found. It may occasionally bite humans whose dwellings are infested by bats. Distributed throughout the U.S., records from the northeast include Pennsylvania, New York, and Connecticut.

Imported ticks

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Travelers abroad have found exotic ticks on themselves after returning to the United States. Other ticks may be imported on pets and other animals. Some of these ticks are potential vectors of pathogens of domestic livestock and introduction and establishment of these ticks would have serious consequences for the livestock industry. For humans, there are a number of bacterial and rickettsial pathogens and encephalitis and hemorrhagic fever viruses carried by ticks in Europe, Asia, Africa and Australia. For example, cases of boutonneuse fever, also called Mediterranean spotted fever, have occurred in travelers returning to the U.S. Boutonneuse fever is distributed through Africa, countries around the Mediterranean, southern Europe, and India. Other spotted fever diseases are African tick-bite fever, Siberian tick typhus, and Queensland tick typhus. Several tick-borne encephalitis viruses, as well as Lyme disease spirochetes, are transmitted by Ixodes ricinus ticks in the British Isles, central and Eastern Europe, and Russia and by Ixodes persulcatus from central Europe, Russia, parts of China, and Japan. The following ticks have been documented from traveler’s returning to the northeast (destination, origin): Amblyomma cajennense (CT, Jamaica), A. hebraeum (CT, South Africa), A. variegatum (NY, Kenya), Rhipicephalus simus (CT, Kenya), Dermacentor auratus (ME, Nepal), and Hyaloma marginatum (CT, Greece). The Connecticut 18 travelers returning from South Africa and Kenya were physician diagnosed with boutonneuse fever. Tick Amblyomma hebraeum, one exotic species that bite prevention measures should be taken by has been imported into the U.S. Found throughout travelers to potentially tick infested areas abroad. southern Africa, it is a vector for Rickettsia Physicians should consider exotic tick-associated conori, the agent of boutonneuse fever. (J. Occi). diseases in the differential diagnosis for a patient with a travel with a travel history outside the United States.

Louse Flies of Deer May Be Confused with Ticks These flies are tick-like, blood-feeding parasitic flies (family Hippoboscidae), which may be confused with true ticks. The adult flies are dorsally flattened like a tick, with short legs. Several species are common parasites of white-tailed deer in the U.S. and are frequently seen by hunters or others in close association with deer. One species, Lipoptena cervi is known as the “deer ked” and was imported from Europe. It occasionally will bite humans. Other “deer keds” are native to the U.S. The female fly retains the larvae, nourishing them internally, and then lays mature larvae, which promptly pupate. The hippoboscid flies associated with deer have wings when they emerge, but lose them once they find a host.

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Tick-Associated Diseases There are at least eleven recognized human diseases associated with ticks in the United States, seven or eight of which occur in the mid-Atlantic or northeastern states. Each of the diseases is highlighted in this section of the handbook. The greatest attention is given to Lyme disease, ehrlichiosis, and babesisois. Although each is a zoonotic vector-borne disease, not all are caused by an infectious agent or are exclusively tick transmitted. A toxin causes tick paralysis, tularemia can be transmitted through contaminated animal tissue or other materials, and babesisois and ehrlichiosis can be transmitted perinatally and through blood transfusion. Tick associations with other pathogens like Bartonella or Mycoplasma are not yet clearly defined. The causative pathogens transmitted to humans by the tick vector are maintained in a reservoir host. Ixodes ticks can be infected with more than one agent and co-transmission and infection can occur. Alternatively, multiple infections can occur from multiple tick bites. In a Connecticut and Minnesota study, 20% of Lyme disease patients also had serological evidence of exposure to another tick-borne agent. Table 2. Tick-associated diseases in the United States. Disease Babesiosis Colorado tick fever Ehrlichiosis, monocytic Ehrlichiosis, granulocytic Lyme disease Southern rash illness Powassan encephalitis Rocky Mountain spotted fever Tick-borne Relapsing Fever Tularemia Tick paralysis

Pathogen or causal agent Babesia microti, Babesia spp. CTF virus (Retoviridae) Ehrlichia chaffeensis Anaplasma phagocytophilum Borrelia burgdorferi Borrelia lonestari (?) Powassan virus Rickettsia rickettsia Borrelia species Franciscella tularensis Toxin

Tick Vector I. scapularis, I. pacificus D. andersoni A. americanum I. scapularis, I. pacificus I. scapularis, I. pacificus A. americanum I. cookei D. variabilis, D. andersoni Ornithodoros species ticks D. variabilis, A. americanum, others D. variabilis, D. andersoni

Lyme disease, monocytic and granulocytic ehrlichiosis, Rocky Mountain spotted fever, and tularemia are nationally reportable diseases. The amount and quality of surveillance data provided to state health departments and then to CDC is quite variable. Most surveillance is passive, dependent upon physician reporting. Most diseases are greatly underreported. Active surveillance or laboratory-based reporting may also exist in some states or areas. Case reports are based on a standardized surveillance case definition, which is not meant to be the basis for diagnosis. An increase in case reports can represent a true increase in disease or increased awareness of the disease and increased reporting. Conversely, a decrease may represent a change in reporting or a lack of reporting, rather than a true decrease in the incidence of disease. Nevertheless, surveillance case reports generally provide valuable long-term tracking of disease trends and may be useful for targeting intervention strategies.

Lyme Disease Lyme disease is the leading arthropod-associated disease in the United States and is caused by the spirochete Borrelia burgdorferi, a corkscrew-shaped bacterium. It is associated with the bite of certain Ixodes ticks, particularly the blacklegged tick, I. scapularis, in the northeastern and northcentral United States and the western blacklegged tick, Ixodes pacificus, on the Pacific Coast. Other Ixodes ticks spread the disease in Europe and Asia. The disease has been reported from 49 states, as well as parts of Canada, and across Europe and Asia. Lyme disease was first recognized as a distinct clinical entity in a group of arthritis patients from the area of Lyme, Connecticut in 1975. In 1981, Dr. Willy Burgdorfer discovered spirochetes 15

in the mid-gut of some I. scapularis ticks from Long Island, New York and the bacteria were later named after him. A Lyme disease testing program by the Connecticut Agricultural Experiment Station and Connecticut Department of Public Health found the greatest prevalence in Connecticut in 1984 and 1985 was in towns east of the Connecticut River (map below right). The distribution of the tick and the risk of disease have since expanded dramatically (see map next page). Nationally, 17,739 human cases were reported in 2000, 17,029 cases were reported in 2001 and 23,763 cases were reported in 2002. Twelve states accounted for 95% of reported cases. In order of incidence in 2002 they were Connecticut, Rhode Island, Pennsylvania, New York, Massachusetts, New Jersey, Delaware, New Hampshire, Wisconsin, Minnesota, Maine, and Maryland. Lyme disease is underreported and these numbers may represent only 1020% of diagnosed cases. National statistics are available through the CDC website, www.cdc.gov and local statistics may be available through state public health departments or on their websites. Lyme disease affects all age groups, but the greatest incidence of disease has been in children under 14 and adults over 40 years of age. In most cases, Lyme disease symptom onset occurs during the summer months when the nymphal stage of the blacklegged tick is active (see prevention).

The spirochete Borrelia burgdorferi (CDC)

160 CT RI NY NJ MA PA

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Incidence per 100,000 population

Incidence of Lyme disease per 100,000 population by selected northeastern states, 1990-2002. Connecticut and Rhode Island have had the highest incidence of disease, while New York, Connecticut, Pennsylvania, and New Jersey have had the largest number of reported cases.

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120 100 80 60 40 20 0 1990

1992

1994

1996

1998

Year

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2000

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2004

Clinical signs and symptoms of Lyme disease Lyme disease is a multisystem disorder with diverse cutaneous, arthritic, neurologic, cardiac, and occasional ocular manifestations. Symptoms that occur within days or weeks following the tick bite reflect localized or early-disseminated infection. Late manifestations become apparent months or years after infection. The major signs and symptoms provided below do not cover all those associated with infection by B. burgodorferi. Those who want additional information can consult the literature provided in the bibliography.

Localized infection •

Lyme disease is characterized in the majority of patients (70-90%) by an expanding red rash at the site of the tick bite called erythema migrans (or EM). Therefore, the rash serves as a clinical marker for early disease, although the presence of a rash may go unrecognized.

•

Erythema migrans may appear within 3 to 30 days (typically 8 or 9 days) after the tick bite. The rash gradually expands over a period of days to a week or more at a rate of ½ to ¾ inch per day and should not be confused with the transient reaction to a tick bite.

•

Rashes vary in size and shape, and may occur anywhere on the body, although common sites are the thigh, groin, trunk, and axilla. Many rashes reach about 6 inches in diameter, but some can expand to 8-16 inches or more. The CDC surveillance case definition

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specifies that an EM rash must be 2.5 inches or greater in diameter (this definition should not be used as diagnostic criteria). •

•

An EM may be warm to the touch, but it is usually not painful and is rarely itchy. Swelling, blistering, scabbing or central clearing occur occasionally. The "bull’s-eye" appearance usually is noted in less than half the cases and is characteristic of older rashes. The EM will resolve spontaneously without treatment.

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Mild nonspecific systemic symptoms may be associated with the rash in about 80% of cases and include fatigue, muscle and joint pain, headache, fever, chills, and stiff neck. These flu-like symptoms may occasionally occur in the absence of an identified rash and be identified as ‘summer flu.’ Respiratory or gastrointestinal complaints may occur, but are infrequent. 22

Below: Lyme rash (EM) 5 days (left) and 10 days (right) on antibiotic treatment. The rash on the left is the same as above. The rash right is the same EM illustrated on the previous page.

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Early disseminated infection Lyme disease spirochetes disseminate from the tick bite site through the skin, lymph, or blood to various organ systems, particularly skin, joint, nervous or cardiac tissue. Signs and symptoms may be intermittent, migratory and changing. Nonspecific viral-like symptoms generally mark early-disseminated infection and up to a fourth of patients may develop multiple secondary rashes. Days or weeks after the bite of an infected tick, migratory joint and muscle pain (also brief, intermittent arthritic attacks), debilitating malaise and fatigue, neurologic or cardiac problems may occur. The symptoms appear to be from an inflammatory response to active infection. Multiple EM, headache, fatigue, and joint pain are the most common clinical manifestations noted in early-disseminated disease in children. Multiple components of the nervous system can be affected by B. burgdorferi. Early neurologic symptoms develop in about 15% of untreated patients and these can include Bell’s palsy (paralysis of facial muscles), meningitis (fever, stiff neck, and severe headache), and radiculoneuropathy (pain in affected

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nerves and nerve roots, can be sharp and jabbing or deep). Children present less often with facial palsy and more commonly with fever, muscle and joint pain, and arthritis (primarily the knee). Carditis (various degrees of heart block) and rhythm abnormalities may occur in 8% or less of patients. Ocular manifestations may include conjunctivitis and other inflammatory eye problems. Antibodies to B. burgdorferi are usually detectable in tests during these manifestations.

Late disseminated infection A year or more after the bite of an infected tick, symptoms of persistent infection in untreated or inadequately treated individuals may include numbness or tingling of the extremities, sensory loss, weakness, diminished reflexes, disturbances in memory, mood or sleep, cognitive function deficits, and an intermittent chronic arthritis (typically swelling and pain of the large joints, especially the knee). Approximately 50-60% of untreated individuals develop arthritis and about 10% of these will progress to chronic arthritis. Attacks of arthritis may last weeks to months with remissions and relapses over a period of several years. The course and severity of Lyme disease is variable. Mild symptoms may go unrecognized or undiagnosed and some individuals may be asymptomatic (no early illness). The EM rash or subsequent arthritic, cardiac or nervous system problems may be the first or only sign of Lyme disease. Most symptoms eventually disappear, even without treatment, 25 although resolution may take months to over a year. The disease can also be chronic and debilitating with occasional permanent damage to nerves or joints, but is rarely, if ever, fatal. Chronic Lyme disease or post-Lyme disease syndrome is a controversial and unclear constellation of symptoms related to or triggered by infection with B. burgdorferi. Disease persistence might be due to a slowly resolving infection, residual tissue damage, inflammation from remains of dead spirochetes, immune-mediated reactions in the absence of the spirochete, co-infection with other tick-borne pathogens, or an alternative disease process that is confused with Lyme disease.

Diagnosis and treatment of Lyme disease A physician should be consulted if Lyme disease is suspected. In the absence of an EM rash, Lyme disease may be difficult to diagnose because its symptoms and signs vary among individuals and can be similar to those of many other diseases. Conversely, other arthritic or neurologic diseases may be misdiagnosed as Lyme disease. Lyme disease is probably both over-diagnosed and underdiagnosed with some patients without Lyme disease convinced they have it and other patients with the disease

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being told they do not have it. A diagnosis of Lyme disease is based primarily on objective clinical findings. A blood test to detect antibodies to Lyme disease spirochetes (serological testing) can aid or support the diagnosis of the disease. Antibodies to Borrelia antigens (parts of the bacteria recognized by the immune system) can usually be detected 3-4 weeks after infection. These tests are not reliable enough to be used as the sole criterion for a diagnosis, however, especially during the early stages of the disease. Tests can give false-negative and false-positive results. Newer tests are more specific, greatly reducing false positive reactions. Reliability of the test improves dramatically in the later stages of the disease as serological reactivity increases, although inaccurate results may still occur. Patients with acute or chronic neurologic or arthritic Lyme disease almost always have elevated antibody levels. Two stage serological testing for Lyme disease is suggested by many public health organizations: •

Stage One: A relatively sensitive first test by enzyme-linked immunosorbent assay (ELISA) or indirect fluorescent antibody (IFA) test. If negative, no further testing is done. Testing at the time of the Lyme disease rash is unnecessary as many will be negative. Antibiotic treatment early in infection may abrogate the antibody response. An ELISA test provides a quantitative measure antibody levels (measurable color reaction) and for rapid testing of large numbers of samples. An ELISA test measures the reaction to all the antigens in disrupted Borrelia or to recombinant antigens, but does not allow identification of which antigens are being bound by antibody and can yield false positives from cross-reactive antibodies. ELISA tests using the C6 peptide of the VslE protein, another protein in B. burgdorferi that elicits a strong response by the immune system, may be as sensitive and selective as the two stage testing procedure.

•

Stage Two: If the first test is positive or equivocal, a more specific Western immunoblot test is performed to simultaneously demonstrate an antibody response to several B. burgdorferi antigens (i.e., proteins recognized by the immune system), which show up as bands on the blot. The Lyme disease spirochete has numerous immunogenic proteins including outer surface proteins (OspA, OspB, and OspC), the 41 kDa antigen on the flagellum, and at least 9 other prominent antigens. The Western blot is labor intensive and requires a subjective interpretation of the results. Although there is an established criterion for a positive blot, there is some disagreement on the number and specific “bands” required for a positive test.

Lyme disease can be treated with one of several antibiotics, including, doxycycline, amoxicillin, cefuroxime axetil, penicillin, ceftriaxone, or cefotaxime. The standard course of treatment is for 14-28 days, depending upon clinical manifestation and drug, though a physician may elect a longer course of treatment. Patients treated in the early stages of the disease usually recover rapidly and completely with no subsequent complications. Oral antibiotics are effective in treating most cases of Lyme disease. Intravenous antibiotics are indicated for central nervous system involvement and for recurrent arthritis. Full recovery is likely for patients treated in the later stages of the disease but resolution of some symptoms may take weeks even with appropriate treatment. Persistence of some symptoms and inability to determine if the bacteria are eliminated can make decisions on the length of treatment difficult. Courses of antibiotics may have health consequences due to the disruption of the normal intestinal bacteria, allergic reactions, increased sun sensitivity (with doxycycline), gall bladder problems (with ceftriaxone), and infection risks with catheters (extended intravenous antibiotics). Treatment failure may result from incorrect treatment, long delay before treatment, misdiagnosis (not Lyme disease), poor treatment compliance by the patient (did not finish the full course of antibiotics), and infection or co-infection with other tickborne agents (i.e., Babesia or Anaplasma). Concurrent babesiosis or ehrlichiosis should be

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considered in patients with a flu-like illness, particularly fever, chills, and headache, that fails to respond to antibiotic therapy for Borrelia. Immunity is insufficient to prevent new infections of Lyme disease with subsequent tick bites that require another course of treatment. Antibody levels generally will decline after treatment, although they may persist for months in some patients after symptoms have resolved.

Southern Tick-Associated Rash Illness (STARI) A Lyme-like rash has been noted following the bite of the lone star tick, A. americanum, in south central and southeastern states and given the name Southern tick-associated rash illness (STARI). The rash is indistinguishable from the rash caused by B. burgdorferi. Little is known about this illness. While spirochetes have been observed in about 1-3% of lone star ticks, the bacteria cannot be cultured in the media used for B. burgdorferi. A spirochete named Borrelia lonestari has been identified in A. americanum by DNA analysis and has recently been cultured in tick cell lines.

Human Babesiosis Human babesiosis is a malaria-like illness that is caused by protozoa found in the red blood cells of many wild and domestic animals. Babesiosis is caused by Babesia microti in the northeast and upper midwest United States. Babesia microti is a parasite of white-footed mice, as well as voles, shrews, and chipmunks. Other species or variants of Babesia are associated with human disease in other parts of the United States (i.e., California and Missouri), Europe, and Asia. Human babesiosis has been recognized since Babesia microti in red blood cells (CDC). the early 1970’s in parts of Massachusetts (particularly Nantucket Island), Block Island, Rhode Island, and the eastern parts of Long Island, New York. Most cases in Rhode Island are reported from the southern coastal regions. The first Connecticut case of human babesiosis was reported from Stonington in 1988 and the majority of cases continue to be reported from the southeastern portion of that state, although recent evidence indicates that the organism has become more widely distributed in the state. The number of confirmed cases has increased in New Jersey in recent years, which may represent increased risk or increased awareness. The disease is reportable in only a few states. The number of reported cases is probably only a small fraction of clinically diagnosed cases with many other subclinical or mild cases going undetected and unreported. Nevertheless, the distribution and number of cases of babesiosis appears to be increasing. Table 3. Number of reported human cases of babesiosis in select northeastern states, 1997-2001 (compiled from state health department web sites or reports). State CT RI MA NY NJ

1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 31 45 40 52 56 69 2 6 18 35 27 19 66 51 8 18 26 107 61 72 3 7 3 15 19

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The white-footed mouse is the primary reservoir for B. microti, which is transmitted by I. scapularis. While data on the prevalence of infection in P. leucopus and particularly in I. scapularis is limited to a few studies, babesial parasites have been observed in up to 41% of mice and over 90% can be serologically positive in endemic areas. Infection in mice may be life long. Infections in ticks generally appear to be lower than with B. burgdorferi, but in highly endemic areas tick infection by Babesia species may be equally prevalent. Maintenance of the parasite seems to require moderate to high tick densities. Most human cases occur during the summer months when nymphs of the blacklegged tick are active. Babesia can also be transmitted through blood transfusions from asymptomatic donors. Both the mouse (or other reservoir competent rodent host such as the meadow vole) and the blacklegged tick are required to complete different aspects of the Babesia lifecycle. Larval or nymphal ticks acquire the babesial parasites when feeding on an infected mouse. In the tick gut, male and female gametes unite to form zygotes. Subsequently a stage of the parasite reaches the salivary glands and become dormant until the tick feeds again. The parasite is passed to the next stage of the tick (transstadial transmission). Upon tick attachment, infectious sporozoites are formed and shed in the saliva of the tick. It may require as many as 54 hours of attachment before White-footed mouse with I. scapularis ticks. transmission occurs. Adult I. scapularis also can transmit the parasite. During transmission, the sporozoites enter red blood cells, reproduce asexually, and emerge to invade new cells, destroying the infected cells in the process and causing the symptoms associated with babesiosis. Introduction of B. microti into another mouse perpetuates the cycle. A female tick does not transmit this parasite to her eggs (transovarial transmission). The clinical presentation of human infection ranges from subclinical to mild flu-like illness, to severe life-threatening disease. Infection often is accompanied by no symptoms or only mild flu-like symptoms in healthy children and younger adults. The disease can be severe or fatal in the elderly, the immune suppressed (HIV infection or use of immunosuppressive drugs), and people without spleens. The greatest incidence of severe disease occurs in those older than 40 years of age. Symptoms of babesiosis include fever, fatigue, chills, sweats, headache, and muscle pain beginning 1-6 weeks after the tick bite. Gastrointestinal symptoms (nausea, vomiting, diarrhea, abdominal pain), respiratory symptoms (cough, shortness of breath), weight loss, dark urine, and splenomegaly also may occur. Complications such as acute respiratory failure, congestive heart failure and renal failure have been associated with severe anemia and high levels of infected cells (parasitemia). Up to 80% of red blood cells can be infected in a splenectomized patient, although 1-2% parasitemia is typical in those with intact spleens. Illness may last weeks to months and recovery can take many months. Co-infection with B. microti and B. burgdorferi can result in overlapping clinical symptoms, a more severe illness, and a longer recovery than either disease alone. A specific diagnosis of babesiosis can be made by detection of the parasites in Giemsastained blood smears and confirmed serologically by an indirect fluorescent antibody (IFA) test. A complete blood count (CBC) is useful in detecting the hemolytic anemia and/or thrombocytopenia (decrease in blood platelets) suggestive of babesiosis. Elevated liver function

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tests may be present. The parasite can also be detected by polymerase chain reaction (PCR) assay. The drugs of choice in the treatment of babesiosis are oral clindamycin plus quinine sulfate or a combination of oral azithromycin and atovaquone. Adverse effects (i.e., tinnitus, vertigo, lower blood pressure, gastrointestinal upset) are commonly associated with clindamycin and quinine use and some patients cannot tolerate the treatment. The combination of azithromycin and atovaquone is better tolerated. Severely ill patients should be given intravenous clindamycin and quinine and an exchange blood transfusion. Following drug treatment, the parasites usually are eliminated and there is no recurrence of disease. In immunocompromised individuals, parasitemia may persist for months and possibly years following recovery from illness and relapse may occur. Currently, individuals who have ever been diagnosed with babesisois are excluded from donating blood.

Human Ehrlichiosis The Ehrlichiae are a group of bacteria with several genera and species known to cause disease in dogs, cattle, sheep, goats, horses and humans. These bacteria invade different types of white blood cells (leucocytes) and the disease is often named from the primary type of infected blood cell, including granulocytes or monocytes. Veterinarians have known about canine ehrlichiosis, caused by E. canis and transmitted by the Brown dog tick since 1935. Two principal forms of ehrlichiosis in humans currently are recognized in the United States. Human monocytic ehrlichiosis (HME) is caused by Ehrlichia chaffeensis. Human granulocytic ehrlichiosis (HGE) is caused by Anaplasma phagocytophilum (some cases by Ehrlichia ewingii) and accounts for about two-thirds of all ehrlichiosis cases in the U.S. Surveillance for ehrlichiosis in most states is sparse. Ehrlichiosis was added to the national list of reportable diseases in 1999. In Connecticut, there were 544 confirmed cases of HGE reported from 1995-2002. Cases were distributed across all eight Connecticut counties. In New York, both HGE and HME have been reported mainly from the lower Hudson River Valley and eastern Long Island. Human granulocytic ehrlichiosis was first described from patients in Wisconsin and Minnesota in 1994. The blacklegged tick is the principal vector for HGE (or technically Anaplasmosis) in the northeastern and upper mid-western states. Therefore, most cases of HGE have been reported from states where Lyme disease is highly endemic, particularly Connecticut, New York, and parts of Minnesota and Wisconsin. The western blacklegged tick is the vector in northern California. Laboratory studies indicate transmission can occur within 24 hours of tick attachment and possibly within 8 hours. A single tick has been demonstrated to simultaneously transmit both B. burgdorferi and A. phagocytophilum.

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Human monocytic ehrlichiosis, caused by E. Morulae of A. phagocytophilum in cytoplasm of neutrophil (CDC). chaffeensis, was first recognized in the United States in 1986 in a patient who was bitten by a tick in Arkansas. Lone star ticks are the vector for E. chaffeensis in south central and southeastern regions of the country where most cases of HME occur. The DNA of E. chaffeensis has been detected in lone star ticks from Connecticut and Rhode Island, so cases of HME may occur in southern New England. Most cases of ehrlichiosis occur in May, June, or July with 80-90% of cases occurring between April and September. This corresponds to the activity of nymphal I. scapularis and adult lone star ticks. Symptoms for both types of ehrlichiosis are non-specific and include fever, 23

headache, muscle pain, nausea, vomiting, and malaise. Initial symptoms appear 5-10 days after the tick bite. Illness may be mild, moderate or severe. Some cases require hospitalization and there have been fatalities. A rash is uncommon in adults, but a rash has been observed in many HME cases in children. Most patients show a decrease in their white blood cell (leukopenia) and blood platelet (thrombocytopenia) counts and an increase in liver enzymes. The number of clinical cases increases with age. The highest rates have been observed for patients 50 years of age or older. Severe cases and fatalities have been reported across all age groups. HME has been confused with Rocky Mountain spotted fever (RMSF). There are no absolute clinical criteria to distinguish Human monocytic ehrlichiosis from RMSF although patients with HME are much less likely to have a rash (10-15 percent) and are more likely to be leukopenic. A diagnosis of ehrlichiosis should be considered for patients with a flu-like febrile illness and possible exposure to I. scapularis. Co-infections by the agents of HGE and Lyme disease have been reported and may result in more severe disease. A diagnosis of ehrlichiosis can be confirmed by a serological test, Morulae of E. chaffeensis in observing the organism in white-blood cells, culturing the cytoplasm of monocyte (CDC). organism, or amplification of the DNA of the ehrlichia organism by polymerase chain reaction (PCR). Tests may be negative in the early stages of disease and are more reliable in specimens obtained during the 3 third week of illness. The drug of choice for the treatment of ehrlichiosis is doxycycline (tetracycline may also be used) and should be started upon suspicion or clinical diagnosis of ehrlichiosis. Response to antibiotic therapy is rapid with fever subsiding in 24-72 hours. The use of doxycycline in children under 8 years of age is generally not recommended because it may stain the permanent teeth, but could be used in severe cases. Rifampin has been used successfully when doxycycline cannot be used.

Rocky Mountain Spotted Fever Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii, a type of bacterium that occurs throughout the continental United States, southern Canada, Mexico and Central America and parts of South America. Although the disease was first recognized in 1896 from virulent cases in Idaho and Montana, the name is somewhat misleading as only a small proportion of current cases are reported from the Rocky Mountain region. In the U.S., most cases of RMSF occur in the South Atlantic and West Central states. North Carolina and Oklahoma have the highest rates of RMSF accounting for 35% of the total cases reported to the CDC during 1993-1996. The majority of RMSF cases are associated with the American dog tick. In the western U.S., the vector is the Rocky Mountain wood tick, D. andersoni. RMSF is relatively uncommon in New England. Between 1997 and 2002, based on figures in the CDC’s Morbidity and Mortality Weekly Report (MMWR), approximately 3,520 human cases were reported in the United States, of which 28 (less than one percent) were from New England. More cases of RMSF are reported from the mid-Atlantic states, but these still accounted for only 6.7% of the total. Few ticks are infected. Scientists at the Connecticut Agricultural Experiment

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Station found that less than 1% of 3,000 American dog ticks examined in Connecticut had spotted fever-group organisms, and not all spotted fever group rickettsiae are infectious to humans. Table 4. Number of reported human cases of Rocky Mountain spotted fever in northeastern states, 1997-2002. (Data compiled from MMWR and/or state health department web sites; 2002 numbers provisional. One case was reported from New Hampshire in 2001). State CT RI MA NY NJ PA US total

1997 3 1 1 14 4 9 16 409

1998 1999 2000 2001 2002 2003 2004 2 0 0 0 0 3 0 4 0 0 4 0 2 2 2 6 13 14 9 4 18 12 7 12 9 2 13 18 25 20 20 365 579 495 695 961

2005

2006

Children are particularly at risk for RMSF with two-thirds of the cases in patients under 15 years of age. Like Lyme disease, the highest rate in children is in the 5 to 9 year old age group. Symptoms usually appear within 2 to 9 days after a tick bite. Patients experience a variety of symptoms including sudden fever (90%), severe headache (89%), muscle pain (83%), and rash (78%). The rash may begin as small, pink, non-itchy spots (macules) and then develop into the spotted (petechial) rash characteristic of RMSF. The rash may include the palms (50%) and soles of the feet. The rash may not be present or faint when a physician initially examines a patient. Some patients (10-15%) never develop a rash. The classic spotted rash of RMSF appears after about six days or later. Prompt antibiotic treatment with doxycycline, tetracycline, or chloramphenicol for suspected cases is important because RMSF is fatal in 15-20% of untreated cases. Delays in diagnosis because of the absence of the rash or no knowledge of a tick bite could be dangerous. RMSF is made more severe with inadvertent use of sulfonamides. In recent years, about 1-4% of cases in the U.S. have been fatal. A clinical diagnosis may be confirmed serologically or by PCR, but antibodies may not yet be present when a patient is seen by a physician early in the illness. Below: Examples of spotted fever rash (CDC). Left to right: early (macular) rash on sole of foot, late (petechial) rash on palm and forearm, and rash on hand of a child.

Tick Paralysis A toxin produced by certain Dermacentor ticks during feeding can cause a progressive, ascending paralysis, which is reversed upon removal of the tick. Recovery is usually complete. Paralysis begins in the extremities of the body with a loss of coordination and inability to walk. It progresses to the face with corresponding slurred speech, and finally shallow, irregular breathing. Failure to remove the tick can result in death by respiratory failure. Cases appear more frequently in young girls with long hair where the tick is more easily overlooked. Most cases of tick paralysis are caused by the Rocky Mountain wood tick (Dermacentor andersoni) in northwestern states. The American dog tick has also been known to cause tick paralysis. 25

Tularemia The bacterium, Francisella tularensis, that causes tularemia (Rabbit Fever or Deer Fly Fever) is transmitted by the bite of several species of ticks or bites from deer flies. Ticks associated with tularemia include the American dog tick, D. variabilis; lone star tick, A. americanum; and Rocky Mountain wood tick, D. andersoni. Most cases occur during the summer (May-August), when arthropod transmission is common. The disease also may be contracted while handling infected dead animals (particularly while skinning rabbits), eating under cooked infected meat, or by an animal bite, drinking contaminated water, inhaling contaminated dust, or having contact with contaminated materials. Natural reservoirs of infection include rabbits, hares, voles, mice, water rats, and squirrels. Tularemia was removed from the list of reportable diseases after 1994, but was reinstated in January 2000 because of its potential as a bioterrorism agent. Tularemia occurs throughout the United States. There have been fewer than 200 cases reported each year during the first half of the 1990s and again in 2000 and 2001. Most cases have been reported from the central states of Missouri, Arkansas, and Oklahoma. With the exception of outbreaks of pneumonic tularemia on Martha’s Vineyard that appear related to gardening, landscaping or mowing activities that may have stirred up contaminated dust, reports of this disease are not common in New England, although sporadic cases and outbreaks may occur. There have been pneumonic cases resulting from accidentally running over a rabbit with a lawnmower. All persons are susceptible to tularemia. The clinical symptoms of tularemia depend upon the route of infection. With infection by a tick, an indolent ulcer often occurs at the site of the bite with occasional swelling of the regional lymph nodes. Fever is the most commonly reported symptom. Diagnosis usually is made clinically and confirmed by an antibody test. Antimicrobials with demonstrable clinical 30 activity against F. tularensis include the fluorinated quinolones such as ciprofloxacin as well as streptomycin and gentamicin. While tetracycline or chloramphenicol also may be used, they are less effective and relapses occur more frequently.

Powassan Encephalitis Powassan virus, a Flavivirus, is the sole member of the tick-borne encephalitis (TBE) group present in North America. The disease is named after a town in Ontario, Canada where it was first isolated and described from a fatal case of encephalitis in 1958. Documented cases of Powassan encephalitis (POW) are rare, but the disease may be more common than previously realized. While there were only 27 known cases in North America between 1958-1998 (mainly in Canada and New York state), four additional cases were identified in Maine and Vermont from 19992001 as a result of increased testing for West Nile virus. The ages of these recent New England cases ranged from 25 to 70 years. Previously, the latest recognized symptomatic cases occurred in New York in 1978 and Massachusetts in 1994. POW presents as meningitis or meningoencephalitis progressing to encephalitis with fever, convulsions, headache, disorientation, lethargy, with partial coma and paralysis in some patients. The disease has a fatality rate of 10-15% and may result in severe long-term disability in the survivors. The principal tick vector appears to be Ixodes cookei with cases occurring from May through October.

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Patients generally have a history of tick bite, or a history of exposure to tick habitat or exposure to hosts such as squirrels, skunks, or woodchucks. The blacklegged tick is a competent vector of Powassan virus in the laboratory. A virus very closely related to and apparently a separate subtype of the Powassan virus has been isolated from I. scapularis, but the prevalence and public health significance of this virus is unknown.

Tick-borne Relapsing Fever Soft ticks of the genus Ornithodoros transmit relapsing fever, caused by Borrelia hermsi, or a group of tick-adapted species of the spirochete. Disease is characterized by cycles of high fever and is treated with antibiotics. Relapsing fever ticks are found in rodent burrows, nests, and caves through the western United States. They can live for many years without feeding. Human cases are often associated with people staying in shelters or cabins infested with these ticks. Relapsing fever may be a risk for northeastern residents vacationing or visiting the western U.S..

Colorado Tick Fever Colorado tick fever, caused by a virus, occurs in mountainous areas of the western United States and Canada. There are 200-400 cases each year. Scientists believe cases are underreported. The virus is transmitted by female Rocky Mountain wood ticks. Symptoms begin with an acute high fever, often followed by a brief remission, and another bout of fever lasting 2-3 days. Other symptoms included severe headache, chills, fatigue, and muscle pain. Illness may be mild to severe, but is self-limited and is not fatal. Treatment is symptomatic. Recovery occurs over several weeks but occasionally may take months.

Bartonella Infection The genus Bartonella includes at least 16 species of vector-associated, blood-borne bacteria that infect a wide variety of domestic and wild animals, including rodents. Several are known human pathogens. For example, Bartonella henselae, the agent of cat scratch disease, is transmitted to cats by fleas and generally to humans by bites or scratches from infected cats. The DNA of various Bartonella have been found in ticks, including I. scapularis and I. pacificus, clearly ingested during feeding, but the ability of ticks to transmit these bacteria in the laboratory or field still needs to be determined.

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Lyme Disease in Domestic and Companion Animals Domestic animals (dogs, cats, horses, cows, and goats) can become infected with Lyme disease bacteria and develop clinical disease. Lameness and swollen joints, fever, lymph node enlargement, reduced appetite, and a reluctance to move are the usual symptoms in these animals. Disease is more common in dogs and relatively less frequent in cats. Most dogs in a Lyme disease endemic area will eventually become infected (based on positive serology) due to their high exposure to ticks and some will develop disease each year. Limb and joint arthritis is the most frequent symptom in canine Lyme disease; cardiac, neurological, ophthalmic, and a unique renal involvement is less common. Lyme nephritis in dogs often results in the death of the animal, even with aggressive treatment. Animals are treated with antibiotics (tetracycline or penicillin-group) and nonsteroidal anti-inflammatory drugs for Swollen joints in a dog with Lyme symptomatic relief. Most dogs respond dramatically to disease (31). antibiotic treatment within days and will make a complete recovery. Chronic disease appears rare and a lack of response to therapy may suggest another diagnosis. Other disease processes, which should be ruled out, include rheumatoid arthritis, infectious arthritides, and other tick-borne diseases such as Rocky Mountain spotted fever and ehrlichiosis. However, studies have shown infection and antibody titers may persist in dogs after efficacious treatment. It is not clear if a reoccurrence of disease is due to another tick exposure or from the initial infection. Some data suggests that treatment in the absence of clinical disease for seropositive dogs or those with a history of tick bite may be indicated. Prevention of disease in companion animals is covered in the host management section.

Additional sources of information about tick-associated diseases The Centers for Disease Control and Prevention, National Center for Infectious Diseases, Division of Vector-Borne Infectious Diseases, P.O. Box 2087, Fort Collins, Colorado, 80522 and Division of Viral and Rickettsial Diseases, 1600 Clifton Road, NE, MS G-13, Atlanta, Georgia 30333. The CDC-NCID web site (www.cdc.gov/ncidod/index.htm) provides details on the natural history, epidemiology, signs & symptoms, diagnosis, treatment, prevention & control for several zoonotic diseases. State health departments can provide information on the incidence of Lyme disease and other tick-borne illnesses in the state. There is usually a division or department that handles Lyme disease and other vector-borne diseases. Statistics are sometimes available on a department’s web site. Lyme disease foundations or groups can provide information or patient support. These include the American Lyme Disease Foundation, Inc. (ALDF), Mill Pond Offices, 293 Route 100, Somers, New York 10589 (telephone 914-277-6970, fax 914-277-6974, e-mail: [email protected], web site: www.aldf.com) and the Lyme Disease Foundation (LDF), One Financial Plaza, Hartford, CT 06103 (telephone 860-525-2000, hotline 800-886-LYME, e-mail: [email protected], website: www.Lyme.org).

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Personal Protection Tick Bite Prevention Personal protection behaviors, including avoidance and reduction of time spent in tickinfested habitats, using protective clothing and tick repellents, checking the entire body for ticks, and promptly removing attached ticks before transmission of Borrelia spirochetes can occur, can be very effective in preventing Lyme disease. However, surveys and the continuing incidence of disease suggest that few people practice these measures with sufficient regularity. Preventive measures are often considered inconvenient and, in the summer, uncomfortable. Despite the efficiency of tick repellents, particularly with DEET applied to skin and permethrin applied to clothing, they are under-utilized. Checking for ticks and prompt removal of attached ticks is probably the most important and effective method of preventing infection! Important points to consider in tick bite prevention and checking for ticks include: Tick Behavior •

Most Lyme disease cases are associated with the bite of the nymphal stage of the blacklegged tick, of which 10-36% may be infected with Lyme disease spirochetes.

•

Nymphal blacklegged ticks are very small (about the size of a pinhead), difficult to spot, and are active during the late spring and summer months when human outdoor activity is greatest. The majority (about 75%) of Lyme disease cases are associated with activities (play, yard or garden work) around the home.

•

Adult blacklegged ticks are active in the fall, warmer days in the winter, and in the spring when outdoor activity and exposure is more limited. They are larger, easier to spot, and therefore associated with fewer cases of Lyme disease (even though infection rates are higher).

•

Ticks do not jump, fly or drop from trees, but grasp passing hosts from the leaf litter, tips of grass, etc. Most ticks are probably picked up on the lower legs and then crawl up the body seeking a place to feed. Adult ticks will, however, seek a host (i.e., deer) in the shrub layer several feet above the ground.

•

Children 5-13 years of age are particularly at risk for tick bites and Lyme disease as playing outdoors has been identified as a high-risk activity. Take notice of the proximity of woodland edge or mixed grassy and brushy areas from public and private recreational areas and playing fields. While ticks are unlikely to be encountered in open fields, children chasing balls off the field or cutting through woods to school may be entering a high-risk tick area.

•

Pets can bring ticks into the home, resulting in a tick bite without the person being outdoors. A veterinarian can suggest methods to protect your pets. Engorged blacklegged ticks dropping off a pet will not survive or lay eggs in the house, as the air is generally too dry.

29

32

33

Prevention • Wear light-colored clothing with long pants tucked into socks to make ticks easier to detect and keep them on the outside of the clothes. Unfortunately, surveys show the majority of individuals never tuck their pants into their socks when entering tick-infested areas. It is unclear just how effective this prevention measure is without the addition of a repellent. Larval and nymphal ticks may penetrate a coarse weave sock. Do not wear open-toed shoes or sandals. • Use a DEET or permethrin-based mosquito and tick repellent, which can substantially increase the level of protection (see section on repellents). This approach may be particularly useful when working in the yard, clearing leaves, and doing other landscaping activity with a high risk of tick exposure. A separate set of work or gardening clothes can be set aside for use with the permethrin-based clothing tick repellents. • When hiking, keep to the center of trails to minimize contact with adjacent vegetation. • Unattached ticks brought in on clothing can potentially result in a later tick bite. Blacklegged ticks can survive for many days in the home depending upon the humidity. In the laboratory, nymphal I. scapularis can survive for over 6 months at 93-100% relative humidity (RH), but over half will die in less than 4 days at 65% RH (RH in modern homes is generally 88%) mortality. However, natural pyrethrin with the synergist piperonyl butoxide provided limited tick control in the residential landscape in several trials. By contrast, synergized pyrethrin was more effective when combined with insecticidal soap or as part of a silicon dioxide (from diatomaceous earth) product. Silicon dioxide acts as a desiccant. Thorough coverage appears particularly important with pyrethrin and insecticidal soap products. With the exception of a desiccant, there is little residual activity. At least two applications may be required.

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Table 4. Acaricides with products labeled for the control of ticks in the residential landscape.

Chemical

Some brand or common names*

Chemical type and usage

Bifenthrin

Talstar® Ortho® product

Pyrethroid insecticide. Available as liquid and granular formulations. Products available for homeowner use and commercial applicators.

Carbaryl

Sevin®

Carbamate insecticide. A common garden insecticide for homeowner use, some products are for commercial use only.

Cyfluthrin

Tempo® Powerforce

Pyrethroid insecticide. Available for commercial and homeowner use with concentrates and ready to spray (RTS) products.

Deltramethrin

Suspend® DeltaGard® G

A pyrethroid insecticide for commercial applicators.

lambdacyhalothrin

Scimitar® Demand®

A pyrethroid insecticide for commercial applicators.

Permethrin

Astro® Ortho® products Bonide® products Tengard® SFR Others

Pyrethroid insecticide. There are concentrates and ready to spray (RTS) products. Most are for homeowner use, a few are for commercial use only.

Pyrethrin

Pyrenone® Kicker® Organic Solutions All Crop Commercial & Agricultural Multipurpose Insecticide®

Natural pyrethrins with the synergist piperonyl butoxide (PBO) or insecticidal soap provide limited tick control. A combination of pyrethrin and PBO with either insecticidal soap or silicon dioxide (from diatomaceous earth) was found effective against ticks in one trial.

*Active ingredients and brand names frequently change as new products are registered and others discontinued. New formulations for homeowner use may become available. Mention of a product is for information purposes only and does not constitute an endorsement by the Connecticut Agricultural Experiment Station.

Homeowner Application of Acaricides One option is for the homeowner to make the pesticide application. Anyone applying pesticides to their own property should be familiar with how to read a pesticide label, how to correctly mix the pesticide, and follow the listed precautions in handling and applying the material. The pesticide label provides information on the active chemical ingredients, formulation, pests and sites for which it can be legally used, directions for use, precautions, hazards to humans, wildlife and the environment, and first aid instructions. Always read and follow pesticide label directions and precautions. It is a violation of federal law to use a pesticide in a manner inconsistent with the label. The label will provide an indication of how hazardous a pesticide is by the signal word on the label. Signal words are based on the EPA toxicity class and must be included on pesticide labels. •

Danger-Poison means highly toxic or poisonous through oral or dermal exposure

•

Danger means highly toxic, but may include severe skin or eye irritants

55

•

Warning means moderately toxic or hazardous

•

Caution means slightly toxic or hazardous

•

No signal word means practically nontoxic

Not all brands of a particular pesticide chemical will be labeled for area tick control. Some products may be for application in or on building and their immediate surroundings. Check the label. Homeowner products come in three forms. •

Ready-to-use (RTU) is premixed and applied directly from the existing container. They are used for spot treatments, treatments of individual plants, or treatment of small areas. Some RTU products, for example, are used to control dog ticks indoors or around a dog’s bedding. Ready-to-spray (RTS) products are used for treating larger areas. The container attaches directly to a garden hose for automatic mixing of the water with the concentrate. For example, a ready spray of 2.5% permethrin or 0.75% cyfluthrin is available as a hose end sprayer for the control of I. scapularis and will cover about 5,000 square feet.

•

Concentrates require mixing the product with water and using your own sprayer (pump-up style, hose-end style, or other type sprayer). Homeowner products may contain carbaryl, cyfluthrin, or permethrin.

•

Granules are designed for lawn applications with a hand held or broadcast spreader. The chemical is usually released with addition of water, so granules generally must be watered in. Granules for tick control on the lawn may contain bifenthrin or carbaryl. Appropriate protective gear as directed on the label should be used when applying pesticides. Surveys have shown many individuals fail to take precautions while applying pesticides. Store pesticides in a cool, dry, secure place. Keep them out of the reach of children. An EPA survey found 85% of households had at least one pesticide on the property and 47% with young children (under age 6) stored them within reach of the child. Keep a pesticide in its original container; do not store diluted spray. Either use up the product or properly depose of leftover product through a community household hazardous waste program. Pesticides should never be poured down the sink or toilet. Empty containers should be triple rinsed and placed in the trash. For more information on handling, applying, storing and deposing of pesticides, readers may refer to the EPA’s Citizen’s Guide to Pest Control and Pesticide Safety (available at www.epa.gov).

Commercial Application of Acaricides Another option is to have a licensed commercial pesticide applicator apply the acaricide. Most companies offering tick control services are lawn care, landscape, or tree care companies, but may include some pest control operators (PCOs) in some states, depending upon what licenses the operator has obtained. A survey of commercial applicators in Connecticut in the mid-1990s found that about 16% offered tick control services. The application of pesticides for tick control comprised less than 5% of their business for most companies. Nevertheless, most companies reported that tick control business had increased and a few companies have specialized solely in providing tick control. A follow-up survey by the author in 1999 indicated that 53% were now offering tick control services. A number of companies provide organically oriented pest management services. A company offering commercial application of pesticides must be registered with the state or states in which they conduct business. A pesticide license is required for the commercial application of pesticides or the application of restricted use materials in the area. There must be at least one commercial supervisory pesticide applicator certified in the type of application being

56

made. In Connecticut, for example, a license for ornamental and turf application from the Department of Environmental Protection is required for applying pesticides for tick control in the landscape. Some tree service companies (arborists) also treat for ticks. Although arborists are tested and licensed by the state specifically for arboriculture services, they must also possess an ornamental and turf license to spray for ticks. Consumers should employ individuals who are licensed to spray for ticks and may request to see the license or license number or check with the agency responsible for the state pesticide program to see if the firms are properly registered and licensed. A commercial company should provide a consumer the name of the pesticide product to be used, the active ingredient in the product, the reentry period (the time before family members can safely reenter the treated area), and the form of the pesticide and type of equipment to be used. In most states, companies are required to provide copies of the label and material safety data sheets (MSDS). With this information, additional information can be obtained over the Internet, from local Cooperative Extension offices, state agencies and pesticide alternative groups. Tips on hiring an applicator are available from EPA’s Citizen’s Guide to Pest Control and Pesticide Safety (available at www.epa.gov). Some general guidelines about a pesticide application that homeowners and commercial applicators should be aware of include: •

Many states (including all New England states, New York, New Jersey, Pennsylvania) have notification laws that require customers or adjacent residents receive written notice prior to an urban pesticide application. Usually this notification is provided only to those who request it through a registry.

•

Pesticides should not be applied on windy days (greater than 10 mph) to avoid drift to non-target areas.

•

Before the spraying, the windows and doors of the home should be closed.

•

Pesticides should be kept away from plants and play areas that you do not want treated. Most tick control pesticides are for ornamental and turf use only and are not labeled for use on plants meant for human consumption. Most of these chemicals are toxic to bees and should not be applied to areas with foraging bees.

•

Pesticides should not be applied near (within 25 feet) wetlands (i.e. lakes, reservoirs, rivers, streams, marshes, ponds, estuaries, and commercial fish farm ponds) or near (within 100 feet) coastal marshes or streams. Even organic pesticides are toxic to fish and aquatic invertebrates.

•

Family members and pets, especially cats, should be kept off the treated area for 1224 hours or other specified reentry interval following the treatment (generally until a spray thoroughly dries).

•

Do not water the lawn after the application of a pesticide to avoid run off (there are a few exceptions with some granular products which must be watered in). Do not apply within 24 hours of rain to avoid run-off. Once the pesticide has dried, however, some materials bind tightly to the soil or vegetation and do not readily move or wash off. They will breakdown with exposure to sunlight and soil microbes.

•

Avoid pesticide applications near a wellhead. The shaft of the well should be tightly sealed and the well water source should be isolated from surface water source. Most acaricides used for tick control are water insoluble and pose little risk to wells by leaching through the soil, but direct exposure should be avoided.

•

Many states (including all New England states, New York, New Jersey, Pennsylvania) have laws that require signs to be posted after an urban treatment is made.

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An Acaricide Primer The purpose of this section is to serve as a reference for some basic, general material on the major classes of chemicals used in tick control. More detailed information is available from the EPA, the Cooperative Extension Service, state pesticide agencies, and independent groups, particularly over the Internet. Some sources of information are listed at the end of this section. Acaricides belong to a variety of chemical classes, which differ in their chemistry, mode of action, toxicology, and environmental impacts. They also contain “inert ingredients,” chemicals that carry or enhance the application or effectiveness of the active ingredient (i.e., the actual acaricide). A variety of pesticides are also used in products to control ectoparasites on pets. Some pet care products are available over the counter and others through a veterinarian. • Organophosphates. There were two organophosphate insecticides commonly used for area-wide tick control, chlorpyrifos (i.e., Dursban) and diazinon. The EPA has cancelled the residential use and some agricultural uses of chlorpyrifos and has cancelled the registration of diazinon for lawn, garden, and other residential outdoor use. Residential applications accounted for nearly 75% of the use of diazinon. Products with these chemicals are no longer used for tick control. • Carbamates. Carbaryl (Sevin) is the carbamate used in the control of ticks. Carbaryl is a broad-spectrum compound used for a wide variety of pests on the lawn, on pets, and in the home. Carbaryl in animals is readily broken down and excreted. It does not appear to cause reproductive, birth, mutagenic, or carcinogenic effects under normal circumstances, but it is a suspected endocrine disrupter. Carbaryl is extremely toxic to bees and beneficial insects, is moderately toxic to fish, but is relatively nontoxic to birds. • Pyrethrins. Pyrethrum is a natural insecticide extracted from certain chrysanthemum plants. Natural pyrethrins are a group of six compounds that form the insecticidal constituents of the natural pyrethrum, which is highly unstable in light and air. Natural pyrethrins are considered knockdown agents because they rapidly paralyze insects, but many insects can detoxify the compound and recover. Therefore, pyrethrins are sometimes combined with a synergist. A synergist is a compound that enhances the toxicity of an insecticide, but is not an insecticide itself. The most common synergist used with pyrethrin is piperonyl butoxide, which inhibits the enzymes that breakdown pyrethrin. Pyrethrins also may be combined with insecticidal soaps, spreader sticker agents, silicon dioxide (desiccant) and other agents to enhance the effectiveness of the product. Pyrethrins have little residual effect, being quickly broken down by exposure to light, moisture, and air. • Pyrethroids. Synthetic pyrethroids are derivatives of the natural compounds, chemically modified to increase toxicity and stability. Most of the chemicals used for area-wide tick control are pyrethroids. The pyrethroids are less volatile than the natural compounds and photostable, which provides some residual activity and greater insecticidal activity. Both pyrethrins and pyrethroids are highly toxic to fish and other aquatic organisms, but generally are much less toxic to mammals, birds and other wildlife. Pyrethroids can be skin and eye irritants. Many concentrated pyrethroid formulations are restricted to commercial use by licensed applicators because of their potential impact on aquatic organisms. However, low concentration, ready-to-use products are available for homeowner use. • Inert ingredients. They may be solvents, propellants, spreaders, stickers, wetting agents, or carriers for the active pesticide chemical. Because these compounds are not the active chemical, they are labeled “inert ingredients” or sometimes “other ingredients”. These compounds often make up the major part of a pesticide formulation. In some cases, the

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inert ingredients may be more toxic than the active ingredient. A few examples of inerts include napththalene, petroleum distillates, and the organic solvents xylene and toluene. • Acaricides for control of ticks on pets. Carbaryl and the pyrethroid permethrin are used in several flea and tick control products for dogs. Studies have indicated that use of permethrin products (i.e., K9 Advantix, Kiltix) can prevent the transmission of B. burgdorferi and A. phagocytophilum. Both are topical products applied to spots along or on the back of the animal. They are not for use on cats, as cats are particularly susceptible to pyrethrin poisoning. Fipronil, a phenypyrazole, is the only commercial insecticide of this chemical type. Formulated pet products are available as a spray or topical spot application (Frontline, Frontline Top Spot, Frontline Plus) for long-term control of fleas and ticks on dogs and cats. It is the material used in the Maxforce TMS rodent bait box. Fipronil dissolves in the oils on the skin, spreads over the body, and collects in sebaceous glands and hair follicles for long-term reapplication. It is not affected by bathing or water immersion. Skin irritation may occur. Fleas are killed from 1-3 months, while ticks are killed for about a month. Trizapentadiene or formanidene compounds include one currently used material, amitraz. In livestock, it is used to control ticks, mites, and lice. It is not a skin irritant, is not readily absorbed into tissue, and degrades rapidly in the environment. Amitraz is used in a tick prevention collar for dogs (Preventic), and one study indicated it could prevent transmission of B. burgdorferi. An amitraz product was one of the compounds initially evaluated for the topical treatment of deer to control I. scapularis.

Additional sources of information about pesticides Environmental Protection Agency (EPA) Public Information Center (telephone 202-2602080), National Center for Environmental Publications and Information (telephone 513-4898190), EPA booklets or the EPA web site (www.epa.gov). National Pesticide Information Center (NPIC) (formerly the National Pesticide Telecommunications Network) is a cooperative effort of Oregon State University and the U.S. Environmental Protection Agency (EPA). The toll-free service is staffed 6:30 am – 4:30 pm Pacific time (9:30 a.m. – 7:30 p.m. Eastern time) 7 days week, except holidays (telephone 1-800858-7378). Information provided by the NPIC includes pesticide information, information of recognizing and managing pesticide poisonings, safety information, health and environmental effects, referrals for investigation of pesticide incidents and emergency treatment information, and cleanup and disposal procedures. Pesticide related fact sheets and other information are available at the web site (http://npic.orst.edu/). Their address is NPIC, Oregon State University, 33 Weniger Hall, Corvallis, Oregon 97331-6502. Extension Toxicology Network (EXTOXNET) is a cooperative effort of University of California-Davis, Oregon State University, Michigan State University, Cornell University, and the University of Idaho. Primary files are maintained and archived at Oregon State University. Pesticide Information Profiles (PIPs) and Toxicology Information Briefs (TIBs) provide information on pesticide trade names, regulatory status, acute and chronic toxicological effects, signs and symptoms of poisoning, ecological effects and environmental fate, physical properties, manufacturer, and references (http://ace.orst.edu/info/extoxnet/). State pesticide regulatory agencies can provide information on the laws and regulations governing the application of insecticides, certification of pesticide applicators, and which products are registered for use in the state. Depending upon the state the agency may be associated with the state Department of Agriculture, Consumer Protection, or Environmental Protection.

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Organic Landcare Practices Standards for organic land care practices for design and maintenance of ecological landscapes have been developed and published by the Connecticut and Massachusetts chapters of the Northeast Organic Farming Association (NOFA). Tick IPM practices are covered under pest and wildlife management guidelines. Practices that are preferred to manage ticks would include personal protection measures, making the environment unsuitable for the pest (i.e., landscape modifications), deer resistant plantings (natives recommended), fencing against deer, and herbalbased deer repellents. The use of arthropod pathogens like entomopathogenic fungi (fungi that kill insects), diatomaceous earth, insecticidal soaps and botanical insecticides are allowed under the standards. However, botanicals cannot be formulated with aromatic petroleum distillates. Ammonia or hot sauce based deer repellents are allowed. Prohibited under the organic standards are all synthetic insecticides and piperonyl butoxide as an insecticide synergist, rodenticides containing warfarin, predator urine (due to collection practices), and products containing sewage sludge (e.g., Milorganite).

Biological Control of Ticks Ticks have relatively few natural enemies, but the use of predators, parasites, and pathogens has been examined for tick control. Tick predation is difficult to document and observations are sporadic. Most arthropod predators are non-specific, opportunistic feeders and probably have little impact on ticks. Anecdotal reports suggested that guinea-fowl or chickens may consume ticks and impact local tick abundance. However, there is no good evidence to support this and turkey foraging was not found to reduce the local density of adult ticks. A minute parasitic wasp, Ixodiphagus hookeri, parasitizes blacklegged ticks in a few areas of New England with superabundant deer and tick populations. However, studies indicate that the usefulness of this wasp to control I. scapularis is very limited. Insect parasitic nematodes have been studied as possible biological control agents. Engorged female I. scapularis are susceptible to certain types of nematodes, but these nematodes are too sensitive to the colder autumn temperatures when the ticks are present. The application of entomopathogenic fungi, however, is a promising approach for controlling ticks. Several fungi have been shown pathogenic to I. scapularis. A perimeter treatment of existing commercial formulations of the fungus Beauveria bassiana and with Metarhizium anisopliae at residential sites has been shown to control I. scapularis in small experimental trials. The EPA has approved M. anisopliae for residential outdoor grub and tick control (Tick-Ex, an oil formulation, and Taenure, a granular formulation; Earth BioSciences, Glastonbury, CT). At the time of this writing, additional trials and commercial development are in progress. Entomopathogenic fungi, applied like a traditional pesticide, may be an option in tick management programs, and an oil-free formulation could meet organic standards.

Lyme disease can be a preventable disease! Surveys have consistently shown most residents in Lyme disease endemic areas consider the disease an important or very important issue that poses a high risk to members of their family. A few precautions and the management of infected ticks in the residential or recreational landscape can substantially reduce the risk of Lyme disease and other tick-associated illnesses. Prompt recognition of infection and treatment can prevent more serious manifestations of disease. While education is important to preventing or mitigating disease, landscape and host management practices combined with the judicious use of acaricides can provide excellent tick control with minimal risk or impact to the environment.

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Selected Bibliography and References Ticks and Tick Ecology Anderson, J. F., and L. A. Magnarelli. 1999. Enzootiology of Borrelia burgdorferi in the northeastern and northcentral United States, pp. 385-389. In G. R. Needham, R. Mitchell, D. J. Horn and W. C. Welborne [eds.], Acarology IX: Volume 2, Symposia. Ohio Biological Survey, Columbus. Anderson, J. F. 1988. Mammalian and avian reservoirs for Borrelia burgdorferi [Review]. Ann. N.Y. Acad. Sci. 539: 180-191. Balashov, Y. S. 1972. Bloodsucking ticks (Ixodoidea): Vectors of diseases of man and animals. Misc. Pub. Entomol Soc. Am. 8: 159376. Battaly, G. R., and D. Fish. 1993. Relative importance of bird species as hosts for immature Ixodes dammini (Acari: Ixodidae) in a suburban residential landscape of southern New York state. J. Med. Entomol. 30: 740-747. Durden, Lance A. and James E. Keirans. 1996. Nymphs of the Genus Ixodes (Acari: Ixodidae) of the United States: Taxonomy, Identification Key, Distribution, Hosts, and Medical/Veterinary Importance. Entomological Society of America, Lanham, MD. 95 pp. Donahue, J. G., J. Piesman, and A. Spielman. 1987. Reservoir competence of white-footed mice for Lyme disease spirochetes. Am. J. Trop. Med. Hyg. 36: 92-96. Drummond, Roger. 1998. Ticks and What You Can Do About Them, 2nd ed. Wilderness Press. 74 pp. Ginsberg, Howard S. 1993. Ecology and Environmental Management of Lyme Disease. Rutgers University Press. 224 pp. IJdo, J. W., C. Wu, L. A. Magnarelli, K. C. S. III, J. F. Anderson, and E. Fikrig. 2000. Detection of Ehrlichia chaffeensis DNA in Amblyomma americanum ticks in Connecticut and Rhode Island. J. Clin. Microbiol. 38: 4655-4656. IJdo, J. W., J. I. Meek, M. L. Cartter, L. A. Magnarelli, C. Wu, S. W. Tenuta, E. Fikrig, and R. W. Ryder. 2000. The emergence of another tickborne infection in the 12-town area around Lyme, Connecticut. J. Infect. Dis. 181: 1388-1893. Keirans, J. E., and L. Durden. 2001. Invasion: Exotic ticks (Acari: Ixodidae) imported into the United States. A review and new records. J. Med. Entomol. 38: 850-861. Keirans, James E. and Taina R. Litwak. 1989. Pictorial Key to the Adults of Hard Ticks, Family Ixodidae (Ixodida: Ixodoidea), East of the Mississippi. Journal of Medical Entomology. 16(5): pp 435-448. Keirans, James E. and Lance E. Durden. 1998. Illustrated Key to Nymphs of the Tick Genus Amblyomma (Acari: Ixodidae) Found in the United States. Journal of Medical Entomology. 35(4): pp. 489-495. Lane, R. S., J. Piesman, and W. Burgdorfer. 1991. Lyme borreliosis: Relation of its causative agent to its vectors and host in North America and Europe. Ann. Rev. Entomol. 36: 587-609. LoGiudice, K., R. S. Ostfeld, K. A. Schmidt, and F. Keesing. 2003. The ecology of infectious disease: Effects of host diversity and community composition on Lyme disease risk. Proc. Nat. Acad. Sci (USA). Mather, T. N., M. L. Wilson, S. I. Moore, J. M. C. Ribeiro, and A. Spielman. 1989. Comparing the relative potential of rodents as reservoirs of the Lyme disease spirochete (Borrelia burgdorferi). Am. J. Epidemiol. 130: 143-150. Mather, T. N., S. R. Telford III, A. B. MacLachlan, and A. Spielman. 1989. Incompetence of catbirds as reservoirs for the Lyme disease spirochete (Borrelia burgdorferi). J. Parasitol. 75: 66-69. McDaniel, Burruss. 1979. How to Know the Mites and Ticks. Wm. C. Brown Company Publishers. Dubuque, Iowa. 335 pp. (Out-ofPrint) Oliver Jr., J. H., M. R. Owsley, H. J. Hutcheson, A. M. James, C. Chen, W. S. Irby, E. M. Dotson, and D. K. McLain. 1993. Conspecficity of the ticks Ixodes scapularis and I. dammini (Acari: Ixodidae). J. Med. Entomol. 30: 54-63. Sonenshine, Daniel E. 1991. Biology of Ticks, Volume 1. Oxford University Press. Oxford. 447 pp. Sonenshine, Daniel E. 1993. Biology of Ticks, Volume 2. Oxford University Press. Oxford. 465 pp. Smith, Carroll N., Moses M. Cole, and Harry K Gouck. Biology and Control of the American Dog Tick. USDA Technical Bull. No. 905, January 1946. Smith, R. P., Jr., E. H. Lacombe, R. W. Rand, and R. Dearborn. 1992. Diversity of tick species biting humans in an emerging area for Lyme disease. Am. J. Public Hlth. 82: 66-69. Stafford III, K. C., R. F. Massung, L. A. Magnarelli, J. W. IJdo, and J. F. Anderson. 1999. Infection with agents of human granulocytic ehrlichiosis, Lyme disease, and babesiosis in wild white-footed mice (Peromyscus leucopus) in Connecticut. J. Clin. Microbiol. 37: 2887-2892.

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StaffordIII, K. C., V. C. Bladen, and L. A. Magnarelli. 1995. Ticks (Acari: Ixodidae) infesting wild birds (Aves) and white-footed mice in Lyme, CT. J. Med. Entomol. 32: 453-466. Stafford III, K. C. 1994. Survival of immature Ixodes scapularis (Acari: Ixodidae) at different relative humidities. J. Med. Entomol. 31: 310-314. Stafford III, K. C. 1993. The epizootiology of Lyme disease. Northeast Wildlife 50: 181-189. Strickland, R.K., R.R. Gerrish, J.L. Hourrigan, and G.O. Schubert. 1976. Ticks of Veterinary Importance. USDA, HPHIS, Agric. Handb. No. 485. Telford III, S. R., T. N. Mather, G. H. Adler, and A. Spielman. 1990. Short-tailed shrews as reservoirs of the agents of Lyme disease and human babesiosis. J. Parasitol. 76: 681-683. Telford III, S. R., T. N. Mather, S. I. Moore, M. L. Wilson, and A. Spielman. 1988. Incompetence of deer as reserviors of the Lyme disease spirochete. Am. J. Trop. Med. Hyg. 39: 105–109. Yuval, B., and A. Spielman. 1990. Duration and regulation of the developmental cycle of Ixodes dammini (Acari: Ixodidae). J. Med. Entomol. 27: 196-201.

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Personal Protection, Repellents, Risk and Transmission Cartter, M. L., T. A. Farley, H. A. Ardito, and J. L. Hadler. 1989. Lyme disease prevention - knowledge, beliefs, and behaviors among high school students in an endemic area. Connecticut Medicine 53: 354-356. Consumers Union. 2000. Buzz Off! Consumer Reports June: 14-17. Costello, C. M., A. C. Steere, R. E. Pinkerton, and J. H. M. Feder. 1989. A prospective study of tick bites in an endemic area for Lyme disease. J. Infect. Dis. 159: 136-139. Couch, P., and C. E. Johnson. 1992. Prevention of Lyme disease. Am. J. Hosp. Pharm. 49: 1164-1173. des Vignes, F., J. Piesman, R. Heffernan, T. L. Schulze, K. C. Stafford III, and D. Fish. 2001. Effect of tick removal on transmission of Borrelia burgdorferi and Ehrlichia phagocytophila by Ixodes scapularis nymphs. J. Infect. Dis. 183: 773-778. Falco, R. C. 1996. Duration of tick bites in a Lyme disease-endemic area. Am. J. Epidemiol. 143: 187-192. Falco, R. C., and D. Fish. 1989. Potential for exposure to tick bites in recreational parks in a Lyme disease endemic area. Amer. J. Public Health. 79: 12-15. Fradin, M. S., and J. F. Day. 2002. Comparative efficacy of insect repellents against mosquito bites. JAMA 347: 13-18. Levin, M. L., and D. Fish. 2000. Acquistion of coinfection and simultaneous transmission of Borrelia burgdorferi and Ehrlichia phagocytophila by Ixodes scapularis. Infect. Immun. 68: 2183-2186. Medical Letter Advisory Board. 1985. Insect repellents. Med. Lett. Drugs-Ther. 27: 62-64. Nadelman, R. B., J. Nowakowski, D. Fish, R. C. Falco, K. Freeman, D. McKenna, P. Welch, R. Marcus, M. E. Aguero-Rosenfeld, D. T. Dennis, and G. P. Wormser. 2001. Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite. N. Engl. J. Med. 345: 79-84. Osimitz, T. G., and R. H. Grothaus. 1995. The present safety assessment of deet. J. Am. Mosquito Cont. Assoc. 11: 274-278. Piesman, J., and E. B. Hayes. 2003. How can we prevent Lyme disease? N. Engl. J. Med. 348: 2424-2430. Piesman, J. 2002. Ecology of Borrelia burgdorferi sensu lato in North America, pp. 223-250. In J. S. Gray, O. Kahl, R. S. Lane and G. Stanek [eds.], Lyme Borreliosis: Biology, Epidemiology and Control. CABI Publishing, Wallingford, Oxon, UK. Piesman, J., and M. C. Dolan. 2002. Protection against Lyme disease spirochete transmission provided by prompt removal of nymphal Ixodes scapularis (Acari: Ixodidae). J. Med. Entomol. 39: 509-512. Piesman, J., B. S. Schneider, and N. S. Zeidner. 2001. Use of quantitative PCR to measure density of Borrelia burgdorferi in the midgut and salivary glands of feeding tick vectors. J. Clin. Microbiol. 39: 4145-4148. Piesman, J., T. N. Mather, R. J. Sinsky, and A. Spielman. 1987. Duration of tick attachment and Borrelia burgdorferi transmission. J. Clin. Microbiol. 25: 557-558. Schreck, C. E., D. Fish, and T. P. McGovern. 1995. Activity of repellents applied to skin for protection against Amblyomma americanum and Ixodes scapularis ticks (Acari: Ixodidae). J. Am. Mosq. Cont. Assoc. 11: 136-140. Schreck, C. E., E. L. Snoddy, and A. Spielman. 1986. Pressurized sprays of permethrin or deet on military clothing for personal protection against Ixodes dammini (Acari:Ixodidae). J. Med. Entomol. 23: 396–399. Shadick, N. A., L. H. Daltroy, C. B. Phillips, U. S. Lang, and M. H. Lang. 1997. Determinants of tick-avoidance behaviors in an endemic area for Lyme disease. Am. J. Prev. Med. 13: 265-270. Shapiro, E. D., M. A. Gerber, N. B. Holabird, A. T. Berg, H. M. Feder, G. L. Bell, P. N. Rys, and D. H. Persing. 1992. A controlled trial of antimicrobial prophylaxis for Lyme disease after deer-tick bites. N. Engl. J. Med. 327: 1769-1773.

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Sood, S. K., M. B. Salzman, B. J. Johnson, C. M. Happ, K. Feig, L. Carmondy, L. G. Rubin, E. Hilton, and J. Piesman. 1997. Duration of tick attachment as a predictor of the risk of Lyme disease in an area in which Lyme disease is endemic. J. Infect. Dis. 175: 996-999. Warshafsky, S., J. Nowakowski, R. B. Nadelman, R. S. Kamer, S. J. Peterson, and G. P. Wormser. 1996. Efficacy of antibiotic prophylaxis for prevention of Lyme disease: a meta-analysis. J. Gen. Intern. Med. 11: 329-333.

Tick Distribution, Landscape and Host Management Adler Jr., Bill. 1999. Outwitting Deer. The Lyons Press, New York, New York. 177 pp. Anderson, J. F., R. C. Johnson, L. A. Magnarelli, F. W. Hyde, and J. E. Myers. 1987. Prevalence of Borrelia burgdorferi and Babesia microti in mice on islands inhabited by whitetailed deer. Appl. Environ. Microbiol. 53: 892-894. Borman, F. H., D. Balmori, and G. T. Geballe. 2001. Redesigning the American Lawn: A Search for Environmental Harmony. 2nd edition. Yale University Press. 178 pp. Carroll, M. C., H. S. Ginsberg, K. E. Hyland, and R. Hu. 1992. Distribution of Ixodes dammini (Acari: Ixodidae) in residential lawns on Prudence Island, Rhode Island. J. Med. Entomol. 29: 1052-1055. Daniels, T. J., D. Fish, and I. Schwartz. 1993. Reduced abundance of Ixodes scapularis (Acari: Ixodidae) and Lyme disease risk by deer exclusion. J. Med. Entomol. 30: 1043-1049. Deblinger, R. D., M. L. Wilson, D. W. Rimmer, and A. Spielman. 1993. Reduced abundance of immature Ixodes dammini (Acari: Ixodidae) following incremental removal of deer. J. Med. Entomol. 30: 144-150. DeNicola, Anthony J., Kurt C. VerCauteren, Paul D. Curtis, and Scott E. Hygnstrom. 2000. Managing White-tailed Deer in Suburban Environments: A Technical Guide. Cornell Cooperative Extension, the Wildlife Society, and Northeast Wildlife Damage Research and Outreach Cooperative. 52 pp. Ellingwood, Mark R. and Suzanne L Caturano. 1988. An Evaluation of Deer Management Options. Publication No. DR-11. CT Department of Environmental Protection. 16 pp. (revised and reformatted, NH Fish & Game Dept., 1996). Falco, R. C., and D. Fish. 1988. Prevalence of Ixodes dammini near the homes of Lyme disease patients in Westchester County, New York. Am. J. Epidemiol. 127: 826-830. Hart, Rhonda Massingham. 1997. Deer Proofing Your Yard & Garden. Storey Books. Pownal, Vermont. 155 pp. Hygnstrom, Scott E., Robert M. Timm, and Gary E. Larson, eds. 1994. Prevention and Control of Wildlife Damage. University of Nebraska Cooperative Extension, USDA-APHIS-Wildlife Services, and Great Plains Agricultural Council Wildlife Committee. Levy, S. A., B. A. Lissman, and C. M. Ficke. 1993. Performance of a Borrelia burgdorferi bacterin in borreliosis-endemic areas. J. Am. Vet. Med. Assoc. 202: 1834-1838. Lewis, A. 1997. Butterfly Gardens: Luring Nature's Lovelist Pollinators to Your Yard. Brooklyn Botanic Garden, Inc., Brooklyn, NY. Maupin, G. O., D. Fish, J. Zultowsky, E. G. Campos, and J. Piesman. 1991. Landscape ecology of Lyme disease in a residential area of Westchester County, New York. Am. J. Epidemiol. 133: 1105-1113. McDonald Jr., John E., Mark R. Ellingwood, and Gary M. Vecellio. 1998. Case Studies in Controlled Deer Hunting. Northeast Deer Technical Committee. 16 p. Available from your state wildlife management agency. Solberg, V. B., J. A. Miller, T. Hadfield, R. Burge, J. M. Schech, and J. M. Pound. 2003. Control of Ixodes scapularis (Acari: Ixodidae) with topical self-application of permethrin by white-tailed deer inhabiting NASA, Beltsville, Maryland. J. Vector. Ecol. 28: 117-134. Stafford III, K. C. 2001. An increasing deer population is linked to the rising incidence of Lyme disease. Frontiers Plant Sci. 53: 3-4. Stafford III, K. C. 1993. Reduced abundance of Ixodes scapularis (Acari: Ixodidae) with exclusion of deer by electric fencing. J. Med. Entomol. 30: 986-996. Stafford, K. C., III, and L. A. Magnarelli. 1993. Spatial and temporal patterns of Ixodes scapularis (Acari: Ixodidae) in southcentral Connecticut. J. Med. Entomol. 30: 762-771. Tekulski, M. 1985. The Butterfly Garden. The Harvard Common Press, Harvard, MA. Ward, J.S. Limiting Deer Browse Damage to Landscape Plants. Connecticut Agricultural Experiment Station Bulletin 968, November 2000. Wilson, M. L., S. R. Telford III, J. Piesman, and A. Spielman. 1988. Reduced abundance of immature Ixodes dammini (Acari: Ixodidae) following elimination of deer. J. Med. Entomol. 25: 224-228. Wilson, M. L. 1986. Reduced abundance of adult Ixodes dammini (Acari: Ixodidae) following destruction of vegetation. J. Econ. Entomol. 79: 693-696.

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Tick IPM and Chemical Control Addiss, S. S., N. O. Alderman, D. R. Brown, and J. Wargo. 1999. A survey of private drinking water wells for lawn and tree care pesticides in a Connecticut town. Environmental & Human Health, Inc., North Haven, CT. Allan, S. A., and L. A. Patrican. 1995. Reduction of immature Ixodes scapularis (Acari: Ixodidae) in woods by application of desiccant and insecticidal soap formulations. J. Med. Entomol. 32: 16-20. Curran, K. L., D. Fish, and J. Piesman. 1993. Reduction of nymphal Ixodes dammini (Acari: Ixodidae) in a residential suburban landscape by area application of insecticides. J. Med. Entomol. 30: 107-113. Deblinger, R. D., M. L. Wilson, D. W. Rimmer, and A. Spielman. 1993. Reduced abundance of immature Ixodes dammini (Acari: Ixodidae) following incremental removal of deer. J. Med. Entomol. 30: 144-150. Dolan, M.C., G. O. Maupin, B. S. Schneider, C. Denatale, N. Hamon, C. Cole, N. S. Zeidner, and K. C. Stafford III. 2004. Control of immature Ixodes scapularis (Acari: Ixodidae) on rodent reservoirs of Borrelia burgdorferi in a residential community of southeastern Connecticut. J. Med. Entomol. In Press. Elfassy, O. J., F. W. Goodman, S. A. Levy, and L. L. Carter. 2001. Efficacy of an amitraz-impregnated collar in preventing transmission of Borrelia burgdorferi by adult Ixodes scapularis to dogs. J. Amer. Vet. Med. Assoc. 219: 185-189. Fish, D. 1995. Environmental risk and prevention of Lyme disease. Am. J. Med. 98 (suppl 4A): 2S-9S. Hansen, Michael. 1992. Pest Control for Home and Garden: The Safest and Most Effective Methods for You and the Environment. Consumer Reports Books. Yonkers, New York. 304 pp. (out-of-print) Hayes, E. B., G. O. Maupin, G. A. Mount, and J. Piesman. 1999. Assessing the prevention effectiveness of local Lyme disease control. J. Public Health Mgt. Practice 5: 84-92. Kamrin, Michael A. Editor. 1997. Pesticide Profiles: Toxicity, Environmental Impact, and Fate. CRC Press. 676 pp. Mount, G. A., D. G. Haile, and E. Daniels. 1997. Simulation of management strategies for the blacklegged tick (Acari: Ixodidae) and the Lyme disease spirochete, Borrelia burgdorferi. J. Med. Entomol. 34: 672-683. Olkowski, William, Shelia Daar, Helga Olkowski. 1991. Common Sense Pest Control. The Taunton Press. 715 pp. Ostfeld, R. S., and D. N. Lewis. 1999. Experimental studies of interactions between wild turkeys and black-legged ticks. J. Vector. Ecol. 24: 182-186. Patrican, L. A., and S. A. Allan. 1995. Laboratory evaluation of desiccants and insecticidal soap applied to various substrates to control the deer tick Ixodes scapularis. Med. Vet. Entomol. 9: 293-299. Patrican, L. A., and S. A. Allan. 1995. Application of desiccant and insecticidal soap treatments to control Ixodes scapularis (Acari: Ixodidae) nymphs and adults in a hyperendemic woodland site. J. Med. Entomol. 32: 859-863. Pound, J. M., J. A. Miller, and J. E. George. 2000. Efficacy of amitraz applied to white-tailed deer by the '4-poster' topical treatment device in controlling free-living lone star ticks (Acari: Ixodidae). J. Med. Entomol. 37: 878-884. Pound, J. M., J. A. Miller, J. E. George, and C. A. LeMeilleur. 2000. The '4-Poster' passive tropical treatment device to apply acaricide for controlling ticks (Acari: Ixodidae) feeding on white-tailed deer. J. Med. Entomol. 37: 588-594. Schulze, T. L., R. A. Jordan, R. W. Hung, R. C. Taylor, D. Markowski, and M. S. Chomsky. 2001. Efficacy of granular deltamethrin against Ixodes scapularis and Amblyomma americanum (Acari: Ixodidae) nymphs. J. Med. Entomol. 38: 344-346. Schulze, T. L., R. A. Jordan, and R. W. Hung. 1995. Suppression of subadult Ixodes scapularis (Acari: Ixodidae) following removal of leaf litter. J. Med. Entomol. 32: 730-733. Solberg, V. B., K. Neidhardt, M. R. Sardelis, F. J. Hoffman, R. Stevenson, L. R. Boobar, and H. J. Harlan. 1992. Field evaluation of two formulations of cyfluthrin for control of Ixodes dammini and Amblyomma americanum (Acari: Ixodidae). J. Med. Entomol. 29: 634-638. Stafford, K. C., III, A. J. DeNicola, and H. J. Kilpatrick. 2003. Reduced abundance of Ixodes scapularis (Acari: Ixodidae) and the tick parasitoid Ixodiphagus hookeri (Hymenoptera: Encyrtidae) with reduction of white-tailed deer. J. Med. Entomol. In press. Stafford III, K. C. 2002. Environmental management for Lyme borreliosis, pp. 368. In J. Gray [ed.], Lyme Borreliosis: Biology and Control. CABI Publishing, Oxon, UK. Stafford III, K. C. 1997. Pesticide use by licensed applicators for the control of Ixodes scapularis (Acari: Ixodidae) in Connecticut. J. Med. Entomol. 34: 552-558. Stafford III, K. C. 1991. Effectiveness of carbaryl applications for the control of Ixodes dammini (Acari: Ixodidae) nymphs in an endemic residential area. J. Med. Entomol. 28: 32-36. Stafford III, K. C.. 1989. Lyme disease prevention: Personal protection and prospects for tick control. Conn. Med. 53: 347-351. Wargo, J., N. O. Alderman, and L. Wargo. 2003. Risks from lawn-care pesticides including inadequate packaging and labeling, pp. 96. Environmental and Human Health, Inc., North Haven, CT. Wilson, M. L., and R. D. Deblinger. 1993. Vector management to reduce the risk of Lyme disease, pp. 126-156. In H. S. Ginsberg [ed.], Ecology and Environmental Management of Lyme Disease. Rutgers University Press, New Brunswick, N.J. Zhioua, E., M. Browning, P. W. Johnson, H. S. Ginsberg, and R. A. LeBrun. 1997. Pathogenicity of the entomopathogenic fungus Metarhizum anisopliae (Deuteromycetes) to Ixodes scapularis (Acari: Ixodidae). J. Parasitol. 83: 815-818.

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About the Author Dr. Kirby Stafford is a medical-veterinary entomologist whose research focuses on the ecology and control of the blacklegged tick. He received his B.S. in entomology and M.S. in veterinary entomology from Colorado State University and Kansas State University, respectively, and his Ph.D. in medical/veterinary entomology from Texas A&M University in 1985. After working at Penn State on a poultry pest management project, he joined the Connecticut Agricultural Experiment Station in 1987. Dr. Stafford became Chief Scientist and Head of the Department of Forestry and Horticulture in 1997.

The Nation’s First State Agricultural Experiment Station The Connecticut Agricultural Experiment Station is a state-supported scientific research institution dedicated to improving the food, health, environment and well-being of Connecticut’s citizens since 1875. The Connecticut Agricultural Experiment Station investigates the growth of plants and studies their pests, insects, ticks, soil and water quality, and food safety, and performs analyses for state agencies. Station staff registers and inspect nurseries, certify honeybee colonies, and inspect thousands of individual plants or other regulated material being shipped into or from Connecticut. The Experiment Station first opened its doors in a laboratory in Wesleyan University in Middletown in October 1875. It was moved to Yale University in 1877 and to its current location in New Haven in 1882. Today, the Experiment Station is composed of one administrative and six scientific departments with around 100 scientists, technicians, and support staff. The Experiment Station also operates a 75-acre research farm in Hamden and a farm at its Valley Laboratory in Windsor, Connecticut. Among many information sheets and publications, The Experiment Station’s web page (www.caes.state.ct.us) features this handbook and an extensive electronic Plant Pest Handbook, which covers diseases, insects, cultural and nematode problems of Connecticut. plants.

The Connecticut Agricultural Experiment Station Putting Science to Work for Society Founded 1875

This handbook is available in electronic format at www.caes.state.ct.us

The Connecticut Agricultural Experiment Station prohibits discrimination on the basis of race, color, ancestry, national origin, sex, religious creed, age, political beliefs, sexual orientation, criminal conviction record, genetic information, learning disability, present or past history of mental disorder, mental retardation or physical disability including but not limited to blindness, or marital or family status. To file a complaint of discrimination, write Director, The Connecticut Agricultural Experiment Station, P.O. Box 1106, New Haven, CT 06504 or call (203) 974-8440. CAES is an equal opportunity provider and employer. Persons with disabilities who require alternate means of communication of program information should contact the Station at (203) 974-8446 (voice); (203) 974-8502 (FAX). Printed by Printing Plus, Portland, Connecticut